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Purpose The intensity progression of core stabilization exercises (CSEs) is usually based on personal criteria rather than on objective parameters. To develop exercise progressions for four of the most common CSEs based on the postural control challenge imposed on the participants, and to analyze the effect of participants’ sex and postural control level on these progressions. Methods Seventy-six males and females performed five variations of front bridge, back bridge, side bridge and bird-dog exercises on two force platforms. The mean velocity of the center of pressure displacement was calculated to assess exercise intensity through the measurement of the participants’ body sway (PBS). Results In general, long bridges produced higher PBS than short bridges, bridging with single leg support produced higher PBS than bridging with double leg support and bridging on a hemisphere ball produced higher PBS than bridging on the floor. The most difficult bridging variations were those performed on a hemisphere ball with single leg support. Regarding the bird-dog, two-point positions produced higher PBS than three-point positions and the positions performed on a hemisphere ball produced higher PBS than those performed on the floor. Conclusion The CSE progressions obtained by males and females were very similar. However, the participants with high trunk control showed less significant differences between exercise variations than the participants with low trunk control, which shows the need to individualize the progressions according to the participants’ training level. Overall, this study provides useful information to guide the prescription of CSE progressions in young physically active individuals.

Background and objectives: Although different variations of the Pallof press exercise are commonly performed in sports and fitness settings to increase core stability, the intensity/difficulty of these variations is unknown and therefore it is difficult to control the training load and establish exercise progressions. This study aimed to compare and rank the postural control challenge imposed by five different isometric variations of the Pallof press exercise through a smartphone accelerometer placed on the participants’ pelvis and to explore sex differences in the lumbopelvic postural control during the exercise performance. Materials and Methods: Twelve physically active participants completed two testing sessions in which they performed two sets of five different isometric variations of the Pallof press exercise (changing the body position and/or the support surface: kneeling on a foam pad, feet together standing on the floor, tandem stance on the floor, feet together standing on a hemisphere ball, and tandem stance on a hemisphere ball). After confirming the acceleration data reliability (intraclass correlation coefficients ≥ 0.72 and typical errors ≤ 17%), a repeated measure ANOVA was carried out to classify the Pallof press variations according to the postural control challenge imposed on the participants and to analyze sex differences on postural control. Results: Significant effects were found for the within-subject factor exercise variations but not for the between-subject factor sex. Pairwise comparisons showed that the exercise variations performed on the hemisphere ball (feet together standing: 0.55 m/s2; tandem stance: 0.61 m/s2) imposed higher postural control demands than those performed on the other surfaces (kneeling on a foam pad: 0.17 m/s2; feet together standing on the floor: 0.22 m/s2; tandem stance on the floor: 0.31 m/s2). In addition, the tandem stance on the floor produced higher lumbopelvic accelerations than the Pallof press kneeling variation. Conclusions: The Pallof press performance in standing rather than kneeling (i.e., reducing the base of support and raising the center of gravity and the height of the lateral force applied by the elastic band) and on a hemisphere ball increased the exercise difficulty compared to more stable surfaces. This information could help to modulate the difficulty and establish progressions for this exercise in physically active young males and females.

Objective. To determine whether the -308 TNF-α promoter polymorphism is associated with markers of HIV progression in the South African population. Methods. Polymerase chain reaction-restriction fragment length polymorphism was used to detect the -308 TNF-α polymorphism in 75 patients and 76 healthy controls. Serum TNF-α concentrations were measured using ELISA in each cohort. CD4+ T cell apoptosis and HIV-1 RNA viral load were determined using Annexin-V-FITC assay and Nuclisens Easy Q HIV-1 assay respectively. CD4 + T cell counts were measured flow cytometrically. Results. The frequency of -308 G allele was similar in the HIV-1 and control cohorts. The -308GG genotype was associated with lower TNF-α concentrations and markers of increased HIV progression indicated by higher TH lymphocyte apoptosis, lower TH lymphocyte count and higher plasma viral load, irrespective of treatment. Conclusion. The presence of the TNF-α -308 G allele in HIV-1 patients may be associated with increased risk of HIV-1 progression. Further research is required to investigate the nature of this association. S Afr J HIV Med 2012;13(2):72-77.

Nirmatrelvir is an M pro inhibitor active against SARS-CoV-2 and is given with ritonavir, a pharmacokinetic enhancer. In this double-blind, placebo-controlled trial, nirmatrelvir plus ritonavir, when given within 5 days after symptom onset to patients at high risk for disease progression, decreased the risk of Covid-19–related hospitalization or death by 87.8%.

The sputum specimens were collected from the lower respiratory tract of each patient at admission and the levels of viral nuclei acid were determined by a real-time PCR (RT-PCR) approach and indicated by the cycle threshold (Ct) values of RT-PCR assays [2]. SEE PDF] We found that the viral load of the sputum specimen in the lower respiratory tract tested at baseline is closely related to the severity of COVID-19. In summary, we found a positive association between sputum viral load and disease severity as well as risk of progression.

A central paradigm of immunity is that interferon (IFN)-mediated antiviral responses precede pro-inflammatory ones, optimizing host protection and minimizing collateral damage 1 , 2 . Here, we report that for coronavirus disease 2019 (COVID-19) this paradigm does not apply. By investigating temporal IFN and inflammatory cytokine patterns in 32 moderate-to-severe patients with COVID-19 hospitalized for pneumonia and longitudinally followed for the development of respiratory failure and death, we reveal that IFN-λ and type I IFN production were both diminished and delayed, induced only in a fraction of patients as they became critically ill. On the contrary, pro-inflammatory cytokines such as tumor necrosis factor (TNF), interleukin (IL)-6 and IL-8 were produced before IFNs in all patients and persisted for a prolonged time. This condition was reflected in blood transcriptomes wherein prominent IFN signatures were only seen in critically ill patients who also exhibited augmented inflammation. By comparison, in 16 patients with influenza (flu) hospitalized for pneumonia with similar clinicopathological characteristics to those of COVID-19 and 24 nonhospitalized patients with flu with milder symptoms, IFN-λ and type I IFN were robustly induced earlier, at higher levels and independently of disease severity, whereas pro-inflammatory cytokines were only acutely produced. Notably, higher IFN-λ concentrations in patients with COVID-19 correlated with lower viral load in bronchial aspirates and faster viral clearance and a higher IFN-λ to type I IFN ratio correlated with improved outcome for critically ill patients. Moreover, altered cytokine patterns in patients with COVID-19 correlated with longer hospitalization and higher incidence of critical disease and mortality compared to flu. These data point to an untuned antiviral response in COVID-19, contributing to persistent viral presence, hyperinflammation and respiratory failure. Andreakos and colleagues provide a longitudinal study comparing patients with COVID-19 to patients infected with influenza. They report a dysregulated interferon response whereby IFN-λ and type I IFN production were diminished and delayed in patients with COVID-19, exhibiting a response that is ‘untuned’ with other inflammatory cytokines.

Human cytomegalovirus (HCMV) is a herpesvirus that infects ~60% of adults in developed countries and more than 90% in developing countries. Usually, it is controlled by a vigorous immune response so that infections are asymptomatic or symptoms are mild. However, if the immune system is compromised, HCMV can replicate to high levels and cause serious end organ disease. Substantial progress is being made in understanding the natural history and pathogenesis of HCMV infection and disease in the immunocompromised host. Serial measures of viral load defined the dynamics of HCMV replication and are now used routinely to allow intervention with antiviral drugs in individual patients. They are also used as pharmacodynamic read-outs to evaluate prototype vaccines that may protect against HCMV replication and to define immune correlates of this protection. This novel information is informing the design of randomized controlled trials of new antiviral drugs and vaccines currently under evaluation. In this Review, we discuss immune responses to HCMV and countermeasures deployed by the virus, the establishment of latency and reactivation from it, exogenous reinfection with additional strains, pathogenesis, development of end organ disease, indirect effects of infection, immune correlates of control of replication, current treatment strategies and the evaluation of novel vaccine candidates.Human cytomegalovirus (HCMV) infection is ordinarily controlled by a vigorous immune response; however, HCMV can replicate to high levels and cause end organ disease when the immune system is compromised. In this Review, Griffiths and Reeves discuss HCMV pathogenesis in immunocompromised individuals and emerging strategies to treat and prevent infection and disease.

There is increasing evidence that coronavirus disease 2019 (COVID-19) produces more severe symptoms and higher mortality among men than among women 1 – 5 . However, whether immune responses against severe acute respiratory syndrome coronavirus (SARS-CoV-2) differ between sexes, and whether such differences correlate with the sex difference in the disease course of COVID-19, is currently unknown. Here we examined sex differences in viral loads, SARS-CoV-2-specific antibody titres, plasma cytokines and blood-cell phenotyping in patients with moderate COVID-19 who had not received immunomodulatory medications. Male patients had higher plasma levels of innate immune cytokines such as IL-8 and IL-18 along with more robust induction of non-classical monocytes. By contrast, female patients had more robust T cell activation than male patients during SARS-CoV-2 infection. Notably, we found that a poor T cell response negatively correlated with patients’ age and was associated with worse disease outcome in male patients, but not in female patients. By contrast, higher levels of innate immune cytokines were associated with worse disease progression in female patients, but not in male patients. These findings provide a possible explanation for the observed sex biases in COVID-19, and provide an important basis for the development of a sex-based approach to the treatment and care of male and female patients with COVID-19. Male patients with COVID-19 have higher plasma levels of innate immune cytokines and chemokines such as IL-8, IL-18 and CCL5 and more non-classical monocytes than female patients, whereas female patients mount robust T cell activation maintained even in older age.

Among nonhospitalized patients with Covid-19–related symptoms that began less than a week previously, a 3-day course of remdesivir resulted in an 87% lower risk of hospitalization or death than placebo. Adverse effects in the remdesivir group were similar to those in the placebo group.

Although respiratory failure and hypoxaemia are the main manifestations of COVID-19, kidney involvement is also common. Available evidence supports a number of potential pathophysiological pathways through which acute kidney injury (AKI) can develop in the context of SARS-CoV-2 infection. Histopathological findings have highlighted both similarities and differences between AKI in patients with COVID-19 and in those with AKI in non-COVID-related sepsis. Acute tubular injury is common, although it is often mild, despite markedly reduced kidney function. Systemic haemodynamic instability very likely contributes to tubular injury. Despite descriptions of COVID-19 as a cytokine storm syndrome, levels of circulating cytokines are often lower in patients with COVID-19 than in patients with acute respiratory distress syndrome with causes other than COVID-19. Tissue inflammation and local immune cell infiltration have been repeatedly observed and might have a critical role in kidney injury, as might endothelial injury and microvascular thrombi. Findings of high viral load in patients who have died with AKI suggest a contribution of viral invasion in the kidneys, although the issue of renal tropism remains controversial. An impaired type I interferon response has also been reported in patients with severe COVID-19. In light of these observations, the potential pathophysiological mechanisms of COVID-19-associated AKI may provide insights into therapeutic strategies.Acute kidney injury (AKI) is a common complication of COVID-19. This Review describes current understanding of the pathophysiology of COVID-19-associated AKI, examining potential mechanisms by which SARS-CoV-2 infection might induce direct and indirect effects on the kidney and non-specific factors, including haemodynamic changes and/or organ crosstalk, that may adversely influence kidney function.