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•Body composition and strength remain unclear in transgender women undergoing gender-affirming hormone therapy.•Transgender women tend to adapt their body composition to cis women's bodies.•Changes in strength and muscle mass of trans women could be a risk for sarcopenia.•Nutrition, exercise, or diseases related to the changes in body composition and strength in transgender women should be monitored. Body composition and strength of cisgender (cis) individuals are well established. However, those for transgender women (trans women) undergoing gender-affirming hormone therapy remain unclear. This study aimed to detect possible body composition and strength variations related to sarcopenia. This was a cross-sectional comparative study of 37 trans women, 34 cis men, and 34 cis women. Body composition was measured in all individuals by bioelectrical impedance analysis; prehensile strength by dynamometry was studied in trans women. In this study, trans women had higher body mass index values than cis individuals (P < 0.01). Fat mass was 41% higher for trans women than cis men. Muscle mass (MM) was lower in trans women than cis men (–10%), and higher than cis women (24%). Bone mass was lower in trans women than cis men and higher in cis women (P < 0.01). Trans women's prehensile strengths were 25.26 kg for the right hand and 24.8 kg for the left. Appendicular skeletal muscle mass was 23.63 kg, and appendicular skeletal muscle mass index was 8.14 kg. Trans women undergoing gender-affirming hormone therapy show a tendency to adapt body compartments to those of cis women with increased fat mass and reduced muscle mass. Prehensile strength in trans women was close to the cutoff points for sarcopenia risk. Nutrition, physical activity, strength, and body composition are important to avoid the possible risk for sarcopenia. More studies along these lines are necessary, especially in older adults. [Display omitted]

To analyze the eating habits of the transgender population throughout the transition process, evaluate the nutritional requirements associated with gender transition, and reflect on the possible dietary challenges facing the transgender population. A cross-sectional observational study was carried out with 146 individuals (58.90% transgender women [n = 86] and 41.09% transgender men [n = 60]) aged between 18 and 60 y old. Eating habits and nutritional intake were evaluated through a food consumption frequency questionnaire, 24-h dietary recall, and subsequent data entry using DIAL software. The anthropometric parameters weight and height were determined following the protocol proposed by the International Society for the Advancement of Kinathropometry and waist circumference was determined following the protocol of the World Health Organization. The study found that the diets of the studied population were unhealthy, with low fruit consumption (6.4 ± 4.39 rations in transgender men versus 11.5 ± 2.59 rations in transgender women, P = 0.758898323). Diets were high in lipids (43.62 and 44.24 in transgender women and transgender men, respectively) and protein (16.63 and 15.65 in transgender women and transgender men, respectively). Deficiencies in carbohydrates, folate, vitamin D, and minerals such as calcium, iodine, and zinc were detected along with an excess of selenium and especially phosphorus, which could affect hormone levels. Changes were detected as a result of their desire to look similar physically to the desired sex, they followed rules, ways of acting, and habits of primary socialization (learned in the family during their life). The analysis of the changes observed in our study revealed that during the transition process, eating habits changed based on information, often incorrect, obtained from the internet. Therefore, it is advisable to recommend implementing strategies that increase the consumption of fruits, vegetables and whole grains. In this study, we detected some nutritional deficiencies depending on the type of hormone treatment, so nutritional care must be individualized. Therefore, individualized nutritional interventions focused on increasing the consumption of fruits, vegetables, and whole grains should be carried out. It would be advisable to develop guidelines for nutritional advice, diagnosis, and intervention for transgender people based on scientific evidence as well as provide nutritional advice to the clinicians responsible for their follow-up. •Dietary patterns and hormonal and social factors remain unclear in transgender people undergoing gender-affirming hormone therapy.•Transgender individuals tend to adapt their dietary patterns to look similar physically to the desired sex.•Changes in dietary patterns can have adverse physiological consequences and cause late-onset chronic diseases.•Nutrition, exercise, and diseases related to changes in body composition and strength should be monitored in transgender women.

Nearly half of the human genome is made of transposable elements (TEs) whose activity continues to impact its structure and function. Among them, Long INterspersed Element class 1 (LINE-1 or L1) elements are the only autonomously active TEs in humans. L1s are expressed and mobilized in different cancers, generating mutagenic insertions that could affect tumor malignancy. Tumor suppressor microRNAs are ∼22nt RNAs that post-transcriptionally regulate oncogene expression and are frequently downregulated in cancer. Here we explore whether they also influence L1 mobilization. We show that downregulation of let-7 correlates with accumulation of L1 insertions in human lung cancer. Furthermore, we demonstrate that let-7 binds to the L1 mRNA and impairs the translation of the second L1-encoded protein, ORF2p, reducing its mobilization. Overall, our data reveals that let-7, one of the most relevant microRNAs, maintains somatic genome integrity by restricting L1 retrotransposition. Human Long INterspersed Element class 1 (LINE-1) elements are expressed and mobilized in many types of cancer, contributing to malignancy. Here the authors show that the tumor suppressor microRNA let-7 targets the LINE-1 mRNA and reduces LINE-1 mobilization.

Cardiorenal syndrome type 4 (CRS type 4) occurs when chronic kidney disease (CKD) leads to cardiovascular damage, resulting in high morbidity and mortality rates. Mitochondria, vital organelles responsible for essential cellular functions, can become dysfunctional in CKD. This dysfunction can trigger inflammatory responses in distant organs by releasing Damage-associated molecular patterns (DAMPs). These DAMPs are recognized by immune receptors within cells, including Toll-like receptors (TLR) like TLR2, TLR4, and TLR9, the nucleotide-binding domain, leucine-rich-containing family pyrin domain-containing-3 (NLRP3) inflammasome, and the cyclic guanosine monophosphate (cGMP)–adenosine monophosphate (AMP) synthase (cGAS)–stimulator of interferon genes (cGAS-STING) pathway. Activation of these immune receptors leads to the increased expression of cytokines and chemokines. Excessive chemokine stimulation results in the recruitment of inflammatory cells into tissues, causing chronic damage. Experimental studies have demonstrated that chemokines are upregulated in the heart during CKD, contributing to CRS type 4. Conversely, chemokine inhibitors have been shown to reduce chronic inflammation and prevent cardiorenal impairment. However, the molecular connection between mitochondrial DAMPs and inflammatory pathways responsible for chemokine overactivation in CRS type 4 has not been explored. In this review, we delve into mechanistic insights and discuss how various mitochondrial DAMPs released by the kidney during CKD can activate TLRs, NLRP3, and cGAS-STING immune pathways in the heart. This activation leads to the upregulation of chemokines, ultimately culminating in the establishment of CRS type 4. Furthermore, we propose using chemokine inhibitors as potential strategies for preventing CRS type 4.

Unilateral ureteral obstruction (UUO) is an animal rodent model that allows the study of obstructive nephropathy in an accelerated manner. During UUO, tubular damage is induced, and alterations such as oxidative stress, inflammation, lipid metabolism, and mitochondrial impairment favor fibrosis development, leading to chronic kidney disease progression. Sulforaphane (SFN), an isothiocyanate derived from green cruciferous vegetables, might improve mitochondrial functions and lipid metabolism; however, its role in UUO has been poorly explored. Therefore, we aimed to determine the protective effect of SFN related to mitochondria and lipid metabolism in UUO. Our results showed that in UUO SFN decreased renal damage, attributed to increased mitochondrial biogenesis. We showed that SFN augmented peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) and nuclear respiratory factor 1 (NRF1). The increase in biogenesis augmented the mitochondrial mass marker voltage-dependent anion channel (VDAC) and improved mitochondrial structure, as well as complex III (CIII), aconitase 2 (ACO2) and citrate synthase activities in UUO. In addition, lipid metabolism was improved, observed by the downregulation of cluster of differentiation 36 (CD36), sterol regulatory-element binding protein 1 (SREBP1), fatty acid synthase (FASN), and diacylglycerol O-acyltransferase 1 (DGAT1), which reduces triglyceride (TG) accumulation. Finally, restoring the mitochondrial structure reduced excessive fission by decreasing the fission protein dynamin-related protein-1 (DRP1). Autophagy flux was further restored by reducing beclin and sequestosome (p62) and increasing B-cell lymphoma 2 (Bcl2) and the ratio of microtubule-associated proteins 1A/1B light chain 3 II and I (LC3II/LC3I). These results reveal that SFN confers protection against UUO-induced kidney injury by targeting mitochondrial biogenesis, which also improves lipid metabolism.

Type 4 cardiorenal syndrome (CRS-4) is a pathology in which chronic kidney disease (CKD) triggers the development of cardiovascular disease. CKD pathophysiology produces alterations that can affect the bioenergetics of heart mitochondria, causing oxidative stress and reducing antioxidant glutathione (GSH) levels. GSH depletion alters protein function by affecting post-translational modifications such as S-glutathionylation (RS-SG), exacerbating oxidative stress, and mitochondrial dysfunction. On the other hand, N-acetylcysteine (NAC) is an antioxidant GSH precursor that modulates oxidative stress and RS-SG. Moreover, recent studies have found that NAC can activate the Sirtuin 3 (SIRT3) deacetylase in diseases. However, the role of NAC and its effects on mitochondrial function, redox signaling, and SIRT3 modifications in the heart during CRS-4 have not been studied. This study aimed to investigate the role of NAC in mitochondrial function, redox signaling, and SIRT3 in the hearts of animals with CRS-4 at two months of follow-up. Our results showed that the oral administration of NAC (600 mg/kg/day) improved blood pressure and reduced cardiac fibrosis. NACs’ protective effect was associated with preserving cardiac mitochondrial bioenergetics and decreasing these organelles’ hydrogen peroxide (H2O2) production. Additionally, NAC increased GSH levels in heart mitochondria and regulated the redox state, which coincided with an increase in nicotinamide adenine dinucleotide oxidized (NAD+) levels and a decrease in mitochondrial acetylated lysines. Finally, NAC increased SIRT3 levels and the activity of superoxide dismutase 2 (SOD-2) in the heart. Thus, treatment with NAC decreases mitochondrial alterations, restores redox signaling, and decreases SIRT3 disturbances during CRS-4 through an antioxidant defense mechanism.

Obstructive nephropathy (ON), characterized by urine flow disruption, can induce chronic kidney disease (CKD). Although the release of the obstruction is performed as the primary intervention, renal pathology often persists and progresses. Accordingly, the murine model of releasing unilateral ureteral obstruction (RUUO) is valuable for investigating the molecular events underlying renal damage after obstruction release. Remarkably, after RUUO, disturbances such as oxidative stress, inflammation, lipid accumulation, and fibrosis continue to increase. Mitochondrial dysfunction contributes to fibrosis in the UUO model, but its role in RUUO remains unclear. Additionally, the impact of using antioxidants to restore mitochondrial function and prevent renal fibrosis in RUUO has not been determined. This study aimed to determine the therapeutic effect of pre-administering the antioxidant sulforaphane (SFN) in the RUUO model. SFN was administered 1 day before RUUO to evaluate mitochondrial biogenesis, fatty acids (FA) metabolism, bioenergetics, dynamics, and mitophagy/autophagy mechanisms in the kidney. Our data demonstrated that SFN enhanced mitochondrial biogenesis and reestablished mitochondrial oxygen consumption and β-oxidation. These effects collectively reduced lipid accumulation and normalized mitochondrial dynamics, mitophagy, and autophagy, thereby mitigating fibrosis after obstruction. Our findings suggest that SFN holds promise as a potential therapeutic agent in ON-induced CKD progression in RUUO and opens new avenues in studying antioxidant molecules to treat this disease.

Infection is the leading cause of death in multiple myeloma (MM). However, the cellular composition associated with immune dysfunction is not defined. We analyzed immune profiles in the peripheral blood of patients with MM ( n  = 28) and B-cell chronic lymphoproliferative disorders ( n  = 53) vs. health care practitioners ( n  = 96), using multidimensional and computational flow cytometry. MM patients displayed altered distribution of most cell types (41/56, 73%), particularly within the B-cell (17/17) and T-cell (20/30) compartments. Using COVID-19 as a case study, we compared the immune response to vaccination based on 64,304 data points generated from the analysis of 1099 longitudinal samples. MM patients showed limited B-cell expansion linked to lower anti-RBD and anti-S antibody titers after the first two doses and booster. The percentages of B cells and CD4 + T cells in the blood, as well as the absolute counts of B cells and dendritic cells, predicted vaccine immunogenicity at different time points. In contrast with the humoral response, the percentage and antigen-dependent differentiation of SARS-CoV-2-specific CD8 + T cells was not altered in MM patients. Taken together, this study defined the cellular composition associated with immune dysfunction in MM and provided biomarkers such as the B-cell percentage and absolute count to individualize vaccination calendars.

The Gulf of Mexico is an important crude oil reserve worldwide, and the oyster Crassostrea virginica is an excellent candidate to study the oil spill impacts on marine invertebrates. In this work, the concentrations of polycyclic aromatic hydrocarbons (PAHs) and aliphatic hydrocarbons (AHs) from eight productive oyster areas in the Gulf of Mexico were measured on sediment, water, and tissues from C. virginica . In water, the highest AHs concentration was detected in Tamiahua (0.50 ng/mL), while for PAHs, the highest concentration was > 0.10 ng/mL in Tampamachoco. In sediment, Tamiahua and Tampamachoco lagoons had the highest AHs concentrations with values near 2.5 μg/g dry weight. Considering the PAHs, Tamiahua, Carmen, and Tampamachoco lagoons registered the highest levels, with values > 60 ng/g dry weight. In tissues from C. virginica , La Pesca, Cármen and Mecoacán presented the highest PAHs concentrations with values between 0.20 and 0.25 μg/g dry weight. Furthermore, from the molecular analysis of genes related with different phases of the xenobiotic detoxification process such as hypoxia inducible factor ( hif-1a ), cytochrome P450 10 ( cyp10 ), flavin mono-oxygenase ( fmo ), glutathione S-transferase ( gstΩ1 ), multidrug resistant protein ( mdrd1 ), catalase ( cat ), among others, the differences between lagoons were significant ( P < 0.05) and generally with Las Enramadas showing the highest expression levels. From genes evaluated in this study, hif-1a , cyp10 , fmo , mdrd1 and cat presented the highest expression differentials between lagoons. The above allowed us to validate the utility of molecular markers in the assessment of the hydrocarbons effect on oyster under the conditions from the Southern Gulf of Mexico.

Background/objectives: Fostamatinib is a spleen tyrosine kinase (SYK) inhibitor approved for the treatment of adult patients with chronic immune thrombocytopenia (ITP). There is little information about dose tapering and sustained remission after discontinuation in ITP. In this retrospective multicenter study, we evaluated efficacy and safety of fostamatinib in adult patients with ITP before, during, and after tapering/discontinuation (T/D). Methods: T/D was performed on subjects who achieved complete platelet response (CR) with progressive, conditional dose reduction every four weeks. Results: Sixty-one patients were included from 14 reference centers between October 2021 and May 2023. In subjects that completed T/D (n = 9), the median time from treatment initiation to response was 21 days (IQR: 7.5–42), median time from treatment initiation to CR was 28 days (IQR: 28–42), median time from treatment initiation to the start of tapering was 116 days (IQR: 42–140), and duration of tapering was 112.5 days (IQR: 94.5–191). The median platelet count was 232 × 109/L (IQR: 152–345 × 109/L) at tapering and 190 × 109/L (IQR: 142.5–316.5 × 109/L) at discontinuation. With a median follow-up since discontinuation of 263 days (IQR: 247–313 days), only two patients have relapsed (at 63 and 73 days). Fostamatinib was restarted, achieving a new CR. Platelet counts higher than 100 × 109/L in week 12 were the only positive predictive factors for successful tapering and discontinuation. Conclusions: Sustained response in patient with ITP treated with fostamatinib could be developed. The prognostic factors and recommended scheme of tapering still have to be evaluated.