Joint effects between cadmium exposure and dietary antioxidant quality score on osteoporosis and bone mineral density.

To explore the relationship between dietary antioxidant quality score (DAQS) and Cd exposure both alone and in combination with osteoporosis and bone mineral density (BMD) among postmenopausal women. In total, 4920 postmenopausal women from the National Health and Nutrition Examination Survey were included in this cross-sectional study. Weighted univariate and multivariate logistic regression analyses to assess the association between DAQS and Cd exposure with femur neck BMD, total femur BMD, osteoporosis among postmenopausal women, respectively, and the coexistence effect of DAQS and Cd exposure. Four hundred and ninety-nine had osteoporosis. DAQS (OR = 0·86, 95 % CI 0·77, 0·97) and high DAQS (OR = 0·60, 95 % CI 0·36, 0·99) were found to be associated with decreased odds of osteoporosis, while Cd exposure (OR = 1·34, 95 % CI 1·04, 1·72) and high Cd exposure (OR = 1·45, 95 % CI 1·02, 2·06) were related to increased odds of osteoporosis. A positive correlation was observed between high DAQS and both total femur BMD and femur neck BMD. Conversely, Cd exposure was found to be negatively correlated with total femur BMD and femur neck BMD. Additionally, taking low-Cd and high-quality DAQS group as reference, the joint effect of Cd exposure and DAQS showed greater increased odds of osteoporosis and decreased total femur BMD and femur neck BMD as Cd level and DAQS combinations worsened. There may be an interaction between Cd exposure and DAQS for femur neck BMD, total femur BMD, and osteoporosis in postmenopausal women.

[Establishment and applicability comparison of four models of acute liver ischemia/reperfusion injury in rat].

OBJECTIVE: To clarify the preparation methods of four rat models of liver ischemia/reperfusion injury (IRI) and to determine a liver IRI animal model that is consistent with clinical conditions, has stable pathological and physiological injury, and is easy to operate. METHODS: A total of 160 male Sprague-Dawley (SD) rats were randomly divided into four groups using an interval grouping method: 70% IRI (group A), 100% IRI (group B), 70% IRI with 30% hepatectomy (group C), and 100% IRI with 30% hepatectomy (group D), with 40 rats in each group. Each model was further divided into sham operation group (S group) and ischemia groups of 30, 60, and 90 minutes, with 10 rats in each group. After surgery, the survival status and awakening time of the rats were observed, and the liver lobectomy weight, bleeding volume, and hemostasis time of groups C and D were recorded. Blood samples were collected by cardiac puncture after 6 hours of reperfusion for determination the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), blood urea nitrogen (BUN), serum creatinine (SCr), and γ-glutamyl transpeptidase (γ-GT) in the serum to assess liver and kidney function. Hematoxylin-eosin (HE) staining and immunohistochemical staining of macrophages were performed to analyze the liver tissue structure damage from a pathological perspective. RESULTS: Rats in group A exhibited earlier awakening and acceptable mental status, while rats in the other groups showed delayed awakening and poor mental status. The hemostasis time in group D was approximately 1 second longer than that in group C. The mortality of rats subjected to 60 minutes of 70% hepatic ischemia was 0. Compared to the sham operation group, rats in each experimental group showed significant increases in serum levels of AST, ALT, ALP, BUN, SCr, and γ-GT, indicating impaired liver and kidney function in the rat models of liver IRI. In groups A, B, and C, the 90-minute ischemia subgroup exhibited more pronounced elevation in AST, ALT, ALP, BUN, SCr, and γ-GT levels compared to the 30-minute ischemia subgroup [AST (U/L): group A, 834.94±56.73 vs. 258.74±18.33; group B, 547.63±217.40 vs. 277.67±57.92; group C, 930.38±75.48 vs. 640.51±194.20; ALT (U/L): group A, 346.78±25.47 vs. 156.58±13.25; group B, 408.40±138.25 vs. 196.80±58.60; group C, 596.41±193.32 vs. 173.76±72.43; ALP (U/L): group A, 431.21±34.30 vs. 315.95±15.64; group B, 525.88±62.13 vs. 215.63±17.31; group C, 487.53±112.37 vs. 272.46±92.33; BUN (U/L): group A, 18.35±5.63 vs. 14.32±2.30; group B, 30.21±4.55 vs. 17.41±8.14; group C, 20.50±3.64 vs. 15.93±3.22; SCr (U/L): group A, 27.47±8.91 vs. 22.37±5.66; group B, 43.60±15.57 vs. 36.80±7.95; group C, 63.81±20.24 vs. 42.47±7.03; γ-GT (U/L): group A, 15.64±3.57 vs. 6.82±1.48; group B, 9.28±1.91 vs. 5.62±1.21; group C, 10.98±3.18 vs. 5.67±1.10; all P < 0.05]. The 100% IRI 90-minute group and 100% IRI 90-minute group with 30% hepatectomy exhibited more pronounced increases in the above-mentioned indicators compared to the corresponding 70% IRI control group, indicating increased liver and kidney damage in rats subjected to combined blood flow occlusion and hepatectomy. HE staining showed clear liver tissue structure with intact and orderly arranged cells in the sham operation group, while the experimental groups exhibited cell structure damage, including cell rupture or collapse, cell swelling, nuclear pyknosis, deep cytoplasm staining, cell shedding, and necrosis. The interstitium showed infiltration of inflammatory cells. Immunohistochemical staining revealed a higher number of macrophages in the experimental groups compared to the sham operation group. CONCLUSIONS: Four models of liver IRI in rat were successfully established. As the duration and severity of hepatic ischemia increased, liver cell ischemia worsened, leading to increased hepatocellular necrosis and exhibiting characteristic features of liver IRI. These models can effectively simulate liver IRI following liver trauma, with the group subjected to 100% ischemia and 30% hepatectomy showing the most severe liver injury. The designed models are reasonable, easy to perform, and exhibit good reproducibility. They can be used for investigating the mechanisms, therapeutic efficacy, and diagnostic methods related to clinical liver IRI.

Prediction of anemia using facial images and deep learning technology in the emergency department.

Background: According to the WHO, anemia is a highly prevalent disease, especially for patients in the emergency department. The pathophysiological mechanism by which anemia can affect facial characteristics, such as membrane pallor, has been proven to detect anemia with the help of deep learning technology. The quick prediction method for the patient in the emergency department is important to screen the anemic state and judge the necessity of blood transfusion treatment. Method: We trained a deep learning system to predict anemia using videos of 316 patients. All the videos were taken with the same portable pad in the ambient environment of the emergency department. The video extraction and face recognition methods were used to highlight the facial area for analysis. Accuracy and area under the curve were used to assess the performance of the machine learning system at the image level and the patient level. Results: Three tasks were applied for performance evaluation. The objective of Task 1 was to predict patients' anemic states [hemoglobin (Hb) <13 g/dl in men and Hb <12 g/dl in women]. The accuracy of the image level was 82.37%, the area under the curve (AUC) of the image level was 0.84, the accuracy of the patient level was 84.02%, the sensitivity of the patient level was 92.59%, and the specificity of the patient level was 69.23%. The objective of Task 2 was to predict mild anemia (Hb <9 g/dl). The accuracy of the image level was 68.37%, the AUC of the image level was 0.69, the accuracy of the patient level was 70.58%, the sensitivity was 73.52%, and the specificity was 67.64%. The aim of task 3 was to predict severe anemia (Hb <7 g/dl). The accuracy of the image level was 74.01%, the AUC of the image level was 0.82, the accuracy of the patient level was 68.42%, the sensitivity was 61.53%, and the specificity was 83.33%. Conclusion: The machine learning system could quickly and accurately predict the anemia of patients in the emergency department and aid in the treatment decision for urgent blood transfusion. It offers great clinical value and practical significance in expediting diagnosis, improving medical resource allocation, and providing appropriate treatment in the future.

MiR-146a-5p accelerates sepsis through dendritic cell activation and glycolysis via targeting ATG7.

To unveil the role and regulatory mechanism of miR-146a-5p in sepsis. A sepsis cell model was established via lipopolysaccharide (LPS)-induction in dendritic cells (DCs). The maturation of DCs was evaluated via flow cytometry. Gene expression was measured through reverse-transcription quantitative polymerase chain reaction (RT-qPCR). The concentrations of inflammation biomarkers were revealed via enzyme-linked immunosorbent assay (ELISA). The pathological and histological changes in lungs in the sepsis mice model were analyzed via hematoxylin and eosin (H&E) staining. In this study, the miR-146a-5p level was elevated in the serum of sepsis patients and LPS-induced DCs but decreased in the serums of cured sepsis patients. Furthermore, miR-146a-5p deletion alleviated the activation of T cells and attenuated the imbalance of Th17/Treg. Besides, ATG7 was validated as a target of miR-146a-5p. ATG7 elevation enhanced lactate production and glucose uptake in LPS-triggered DCs. Additionally, upregulation of ATG7 suppressed the protein levels of phosphorylated adenosine monophosphate-activated protein kinase (p-AMPK), phospho protein kinase B (p-AKT), and phosphorylated signal transducer and activator for transcription 3 (p-STAT3). In addition, miR-146a-5p downregulation alleviated T-cell activation, inflammation, lactate production, and glucose uptake in sepsis mice. Moreover, the lung injury due to sepsis was also attenuated as a result of miR-146a-5p silencing. MiR-146a-5p aggravates sepsis through DCs activation and glycolysis via targeting ATG7.

miR-135a-5p mediated down-regulation of STAT6 inhibits proliferation and induces apoptosis of fibroblast-like synoviocytes in rheumatoid arthritis.

OBJECTIVE: Rheumatoid arthritis (RA), as a chronic autoimmune disorder, seriously threatens human health. However, no study has thoroughly illustrated the etiology of RA. The present work focused on investigating the biological functions of STAT6 and the upstream miRNAs that regulate its expression. METHODS: Synovial tissues from rheumatoid arthritis (RA) patients and normal participants were acquired. Cell viability, proliferation, apoptosis, concentrations of cytokines, miRNA and protein levels, and relative luciferase activities were detected. RESULTS: WB and qRT-PCR showed that STAT6 was obviously up-regulated in synovial tissues of RA patients as well as RA fibroblast-like synoviocytes (RA FLSs). Functionally, down-regulation of STAT6 significantly inhibited the growth of RA FLSs as indicated by EdU and CCK-8 assays. In addition, inhibition of STAT6 remarkably promoted apoptosis of RA FLSs. Besides, silence of STAT6 notably suppressed inflammatory cytokine levels, such as TNF-α, IL-6 and IL-1ß. Mechanistically, STAT6 was predicted to be the direct target of and negatively regulated by miR-135a-5p. Moreover, STAT6 was involved in the regulation of miR-135a-5p on cell growth, apoptosis and inflammatory response of RA FLSs. CONCLUSION: miR-135a-5p/STAT6 is a potential novel therapeutic target for RA treatment.

MiR-361-5p promotes proliferation and inhibits apoptosis of fibroblast-like synoviocytes via targeting ZBTB10 in rheumatoid arthritis.

OBJECTIVES: This study is aimed to explore the key role of miR-361-5p in fibroblast-like synovial (FLS) cells of rheumatoid arthritis (RA) and explore the underlying mechanism. METHODS: First, we performed RT-qPCR to evaluate the expression of miR-361-5p in both synovial tissues of RA patients and cultured RA-FLS cells. Then CCK-8 assay, EdU staining, Western blot, flow cytometry, and ELISA were conducted to estimate the influence of inhibiting miR-361-5p on RA-FLS cells. Moreover, we used bioinformatics analysis to predict the potential targets of miR-361-5p and perform a dual luciferase report assay for verification. Finally, rescue experiments were performed to prove the role of miR-361-5p/Zinc Finger And BTB Domain Containing 10 (ZBTB10) in the proliferation, cell cycle, and apoptosis of RA-FLS. RESULTS: We find that the expression of miR-361-5p is increased in both RA tissues and cultured RA-FLS cells. The inhibition of miR-361-5p can not only inhibit proliferation, arrest the cell cycle in G1/G0 phase, and increase apoptosis, but also reduce the inflammatory factors secreted by RA-FLS cells. In addition, ZBTB10 is a direct target for miR-361-5p, over-expression of ZBTB10 reverses the effect of miR-361-5p in RA-FLS. CONCLUSIONS: MiR-361-5p promotes the progression of rheumatoid arthritis by targeting ZBTB10.Key pointsThe influences of miR-361-5p on RA-FLS cells.

MiR-702-3p inhibits the inflammatory injury in septic H9c2 cells by regulating NOD1.

BACKGROUND: Cardiac insufficiency is a common complication of sepsis and septic shock and is the most common cause of death in critically ill patients. Recent studies have found that microRNAs (miRNAs) play a potential role in sepsis as markers, but little is known about their functional effects on sepsis-induced cardiomyopathy (SIC). OBJECTIVE: This study is designed to explore the possible role and underlying mechanisms of miR-702-3p in septic cardiomyopathy. METHODS: As expected, H9c2 cells were induced with lipopolysaccharide (LPS) to construct the model of septic cardiomyopathy. The expression of miR-702-3p was detected by qRT-PCR assay and those of IL-1ß, IL-6 and TNF-α by ELISA assay. The viability, proliferation and apoptosis of LPS-treated H9c2 cells were determined by CCK-8, EdU, flow cytometry and western blot assays. Moreover, Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) was predicted and confirmed as a direct target of miR-702-3p by TargetScan, miRwalk and miRDB prediction and dual-luciferase reporter gene assays. RESULTS: While LPS can weaken the viability of H9c2 cells, miR-702-3p enhances that of LPS-treated H9c2 cells by inhibit the expressions of TNF-α, IL-6, IL-1ß. We found NOD1 is a target gene of miR-702-3p, and over-expression of NOD1 restores the inhibitory effects of miR-702-3p on the LPS-treated H9c2 cells. CONCLUSION: MiR-702-3p played an important role in the pathogenesis of sepsis cardiomyopathy via targeting NOD1, suggesting that miR-702-3p may be a potential new target for the treatment of SIC.

miR-21-5p inhibits inflammation injuries in LPS-treated H9c2 cells by regulating PDCD4.

OBJECTIVES: To explore the expression levels and the potential regulatory mechanism of miR-21-5p in LPS-treated H9c2 cells. METHODS: The secretions of the inflammatory cytokines induced by LPS in H9c2 cells were evaluated using ELISA. We used RT-RCR and western blot to measure the relative mRNA and protein expression levels in LPS-treated H9c2 cells. CCK-8 and EdU assays showed the viability and proliferation profiles of the H9c2 cells. TUNEL assays demonstrated the apoptotic behaviors of the H9c2 cells, and a luciferase reporter analysis was used to investigate the interactions between miR-21-5p and programmed cell death protein 4 (PDCD4). RESULTS: LPS induced damage to the H9c2 cells by reducing the cell viability and down-regulating miR-21-5p. On the other hand, miR-21-5p overexpression inhibited the LPS-induced inflammatory damage in the H9c2 cells. Moreover, PDCD4 was verified as a downstream target gene of miR-21-5p, and its expression was inhibited by the higher miR-21-5p content. Finally, miR-21-5p inhibited septic processes, and the PDCD4 overexpression rescued the miR-21-5p effect in the LPS-treated H9c2 cells. CONCLUSION: Our findings suggest that miR-21-5p inhibits the LPS-induced progression of sepsis in H9c2 cells. Additionally, PDCD4 is a downstream target gene of miR-21-5p, and both molecules serve as potential therapeutic targets for heart sepsis patients.

Exosomes Derived from miR-146a-5p-Enriched Mesenchymal Stem Cells Protect the Cardiomyocytes and Myocardial Tissues in the Polymicrobial Sepsis through Regulating MYBL1.

BACKGROUND: At present, the study has confirmed that the mesenchymal stem cell-derived exosomes (MCSs-Exo) possess cardio-protection in sepsis. Nevertheless, the molecular mechanism of the protection of MSCs-Exo in sepsis remains unknown. Therefore, this research is aimed at studying the molecular mechanism. METHODS: The effects of MSCs-Exo and miR-146a-5p in LPS-induced cardiomyocytes (H9C2 cells) in vitro were verified by CCK-8, EdU assay, flow cytometry, Western blot assay, and RT-qPCR. The effect of MSCs-Exo in vivo was evaluated by CLP-induced sepsis model. The potential gene in MSCs-Exo was verified by bioinformatics analysis, and the potential target of miR-146a-5p was identified by bioinformatics analysis and luciferase reporter assay. At last, the function of miR-146a-5p and its target genes on LPS-induced cardiomyocytes (H9C2 cells) in vitro was validated by recuse experiment. RESULTS: Our findings revealed that MSCs-Exo could effectively protect cardiomyocytes of inflammation model in vitro and myocardial tissues of sepsis model in vivo. Meanwhile, we found that miR-146a-5p was a potential gene in MSCs-Exo, and MYBL1 was the target gene of miR-146a-5p and negatively regulated by miR-146a-5p. In addition, miR-146a-5p overexpression promoted proliferation and inhibited apoptosis of LPS-induced cardiomyocytes. The rescue experiment demonstrated that miR-146a-5p could effectively repress the inflammatory response of cardiomyocytes via decreasing MYBL1 expression. CONCLUSION: This study suggests that miR-146a-5p-bearing MSC-derived exosomes may become an effective treatment for sepsis.

New Construction of Maximum Distance Separable (MDS) Self-Dual Codes over Finite Fields.

Maximum distance separable (MDS) self-dual codes have useful properties due to their optimality with respect to the Singleton bound and its self-duality. MDS self-dual codes are completely determined by the length n , so the problem of constructing q-ary MDS self-dual codes with various lengths is a very interesting topic. Recently X. Fang et al. using a method given in previous research, where several classes of new MDS self-dual codes were constructed through (extended) generalized Reed-Solomon codes, in this paper, based on the method given in we achieve several classes of MDS self-dual codes.

Anxiety and depression correlate with disease and quality-of-life parameters in Chinese patients with ankylosing spondylitis.

AIM: To evaluate the relationship between mental and physical health in Chinese patients with ankylosing spondylitis (AS) and to identify the predictors of psychological status. METHODS: Patients with AS (n=103) and healthy controls (n=121) were surveyed between 2010 and 2011 (cross-sectional study). The Bath Ankylosing Spondylitis Disease Activity Index, Bath Ankylosing Spondylitis Functional Index, Bath Ankylosing Spondylitis Metrology Index, pain visual analog scale, Health Assessment Questionnaire, revised Self-Rating Anxiety Scale, revised Self-Rating Depression Scale, and Short-Form 36 questionnaire were administered. RESULTS: The frequency of anxiety and depression in patients with AS was higher than that in healthy controls (P<0.001). Severe disease status and reduced quality of life (QoL) were associated with anxiety and depression. Disease activity and somatic pain were more severe in the anxious and depressed subgroups. Impaired physical functioning (assessed by Bath Ankylosing Spondylitis Functional Index) was higher in the anxious and depressed subgroups, while measures of spinal mobility (assessed by Bath Ankylosing Spondylitis Metrology Index) were not associated with depression. Lower QoL was observed in the depressed subgroup. CONCLUSION: Low socioeconomic status, lack of health insurance, and fatigue contributed to depression in Chinese patients with AS. These patients may require a psychological care approach that is different from those of other countries.

Body image disturbance and quality of life in Chinese patients with ankylosing spondylitis.

BACKGROUND: Ankylosing spondylitis (AS) is a painful inflammatory disease of the axial skeleton that can cause body image disturbance (BID) and may lead to psychological changes in AS patients. OBJECTIVE: This study investigated the effect of AS patient physical and psychological status on BID and quality of life (QOL). METHODS: Overall, 112 AS patients (84 males, 28 females; mean age, 32.8 ± 10.8) and 127 healthy age-matched individuals (control group; 78 males, 49 females; mean age, 36.9 ± 12.6) were screened for inclusion in the single-centre study. Multiple instruments assessing physical function, psychological function, body image, and QOL were applied. Multivariate stepwise regression analyses were used to determine factors associated with BID, anxiety, and depression. RESULTS: Of 103 AS patients and 121 control subjects, AS patients exhibited greater BID-associated social function, social life, and role function impairments (BID Questionnaire [BIDQ] 2.42 vs. 1.02; 2.20 vs. 1.19; 2.54 vs. 0.72, respectively), lower behavioural avoidance (BIDQ 3.07 vs. 3.49), and similar decreases in vitality and mental health (p < .01). Impaired social function predicted anxiety and depression in AS patients. Disease status (daily activity, general health, and pain) and psychological status (BID, anxiety, and depression) predicted poor QOL (p < .05). CONCLUSION: BID may play a significant role in causing clinical psychological dysfunction in AS patients, including anxiety and depression. Further research is required to fully assess whether these observations are similar in patients with variant AS severity. BID may be useful in clinical prognostic assessment and AS management. PRACTITIONER POINTS: AS patients investigated in this study exhibited BID. There were significant relationships between the BIDQ, disease and psychological variables, and QOL. Disease status, BID, and anxiety and depression indicated a poor QOL.

Human umbilical cord-derived mesenchymal stem cells downregulate inflammatory responses by shifting the Treg/Th17 profile in experimental colitis.

BACKGROUND/AIMS: The aim of this study was to evaluate the effect and mechanisms of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) on immune responses in murine colitis. METHODS: Mice with dextran sulfate sodium (DSS)-induced colitis were injected intraperitoneally with hUC-MSCs or human bone marrow-derived MSCs. The cytokine levels from lamina propria mononuclear cells (LPMCs) and colon tissue were measured using ELISA. Treg and Th17 cells were analyzed using flow cytometry. The proliferation of LPMCs was assessed using Cell Counting Kit-8. RESULTS: hUC-MSCs ameliorate DSS-induced colitis via the downregulation of colon inflammatory responses. Furthermore, hUC-MSCs adjusted modulation of Treg/Th17 cells in the spleen and mesenteric lymph nodes. hUC-MSCs also inhibited LPMCs in vitro. CONCLUSION: hUC-MSCs may be an alternative source of stem cells and are worthy of study in long-term clinical trials.

General transcription factor IIb overexpression and a potential link to proliferation in human hepatocellular carcinoma.

The general transcription factor IIB (TFIIB) plays a central role in preinitiation complex (PIC) assembly, providing a bridge between promoter-bound TFIID and RNA Polymerase II (RNA POLII). TFIIB functionally counteracts the transcriptional activation of hepatitis B virus X protein (HBx), which has been shown to play a role in the development of human hepatocellular carcinoma (HCC). However, the function of TFIIB in HCC remains unclear. In this article, we demonstrate that TFIIB plays an important role in HCC pathogenesis. TFIIB expression was immunohistochemically examined in a series of 100 HCC tissue specimens. The expression level of TFIIB showed significant correlation with the histological grade (P = 0.030), the level of AFP (P = 0.011) and the proliferation marker Ki-67 (P = 0.0002). High TFIIB expression level correlated with poor survival. Western blot analysis also confirmed that the TFIIB protein was overexpressed in HCC tissue compared to benign normal tissue. Additionally, Western blot and qRT-PCR analyses showed a high expression level of TFIIB protein in the HCC cell lines SMMC7721, HepG2, BEL7404, and Huh7 and the immortalized normal line BEL7702 but a lower expression in the normal Chang hepatocyte cell line. Following the release of Huh7 cells from serum starvation, the expression of TFIIB was upregulated. A cell growth assay suggested that TFIIB was involved in the proliferation and growth of HCC cells. In conclusion, our results demonstrate that TFIIB overexpression may play essential roles in the pathogenesis of hepatocellular carcinoma by affecting the proliferation of HCC cells.

A primary analysis of sexual problems in Chinese patients with ankylosing spondylitis.

While the physical impact of ankylosing spondylitis (AS) is central to clinical treatment, the sexual problems associated with AS are often overlooked. Sexual problems may be related to a variety of undocumented demographic parameters, physical impairments, and psychological problems. These associations were examined through a single-center cross-sectional study of 103 AS patients (78 males and 25 females) and 121 healthy individuals (73 males and 48 females). All participants provided information pertaining to sexual problems, sociodemographics, and clinical characteristics via written questionnaires including multiple-choice questions conducted independently in the clinical setting under physician supervision. Rates of both prevalence and severity of sexual dysfunctions in AS patients were much higher than those observed in healthy individuals. Bath Ankylosing Spondylitis (BAS) Disease Activity Index and two parameters of body image disturbance (distress and impairment in social functioning) correlated with impaired partner relationships (P < 0.05). BAS mobility index, impaired social functioning, and BAS functionality index were the most significant causes of impaired sexual function (P < 0.05) in AS patients. Both physical and psychological factors were shown to impact sexual relationships and function in Chinese AS patients. To more effectively manage AS in clinical settings, rheumatologists and nursing specialists should be aware of the condition's impact on sexual health, considering both physical outcomes, such as disease activity and physical function, as well as psychological well-being.