Comparison of cardiovascular disease risk association with metabolic unhealthy obesity identified by body fat percentage and body mass index: Results from the 1999-2020 National Health and Nutrition Examination Survey.

BACKGROUND AND AIM: Cardiovascular disease (CVD) risk among individuals across different categories of metabolic obesity phenotypes is controversial. The study used body fat percentage (BFP) or body mass index (BMI) to categorize obese status and to investigate the association between metabolic obesity phenotypes and CVD risk in a nationally representative population. METHODS: This cross-sectional study included 49463 adult participants in National Health and Nutrition Examination Survey from 1999 to 2020. Metabolic healthy status was defined by the absence of metabolic syndrome according to the revised National Cholesterol Education Program Adult Treatment Group definition. Obesity was identified by BFP, assessed by dual-energy X-ray absorptiometry scan, and BMI. The primary outcome was CVD prevalence. The multivariable logistic regression model and restricted cubic spline analyses were used to examine the associations between metabolic obesity phenotypes and the risk of CVD. RESULTS: Among 49463 adult participants, 32.12% were metabolically unhealthy, 34.10% were overweight, 37.94% were obese; and 8.41% had CVD. Compared with metabolic healthy normal weight, metabolic healthy obesity, and metabolic unhealthy normal weight/overweight/obesity were all associated with increased CVD risk with adjusted odds ratios (95% confidence intervals) of 1.45 (1.14-1.85), 2.80(1.53-5.11), 2.55(1.88-3.47), and 2.96(2.18-4.02), respectively. Nonlinear dose-response relationships between BFP and CVD were observed both in metabolically healthy and unhealthy participants (both P for non-linearity<0.0001). When obesity was defined with BMI, there were a similar prevalence of obesity, and similar associations between metabolic obesity phenotypes and CKD risks. CONCLUSIONS: Metabolic healthy and unhealthy obesity were both associated with higher risks of CVD, whether using BFP or BMI to define obese status. It suggests that metabolic obesity phenotype is a risk factor for CVD.

Ultra-wideband microwave precisely and accurately predicts sheepmeat hot carcase GR tissue depth.

A portable ultra-wideband microwave system (MiS) coupled with an antipodal slot Vivaldi patch antenna (VPA) was used as an objective measurement technology to predict sheep meat carcase GR tissue depth, tested against AUS-MEAT national accreditation standards. Experiment one developed the MiS GR tissue depth prediction equation using lamb carcasses (n = 832) from two slaughter groups. To create the prediction equations, a two layered machine learning stacking ensemble technique was used. The performance of this equation was tested within the dataset using a k-fold cross validation (k = 5), which demonstrated excellent precision and accuracy with an average R2 of 0.91, RMSEP 2.11, bias 0.39 and slope 0.03. Experiment two tested the prediction equation against the AUS-MEAT GR tissue depth accreditation framework which stipulates predictions from a device must assign the correct fat score, with a tolerance of ±2 mm of the score boundary, and 90% accuracy. For a device to be accredited three measurements captured within the same device, as well as measurements across three different devices, must meet the AUS-MEAT error thresholds. Three MiS devices scanned lamb carcases (n = 312) across three slaughter days. All three MiS devices met the AUS-MEAT accreditation thresholds, accurately predicting GR tissue depth 96.1-98.4% of the time. Between the different devices, the measurement accuracy was 99.4-100%, and within the same device, the measurement accuracy was 99.7-100%. Based on these results MiS achieved AUS-MEAT device accreditation as an objective technology to predict GR tissue depth.

Elastin-derived peptides (EDPs) affect gene and protein expression in human mesenchymal stem cells (hMSCs) - preliminary study.

During the aging process, elastin is degraded and the level of elastin-derived peptides (EDPs) successively increases. The main peptide released from elastin during its degradation is a peptide with the VGVAPG sequence. To date, several papers have described that EDPs or elastin-like peptides (ELPs) affect human mesenchymal stem cells (hMSCs) derived from different tissues. Unfortunately, despite the described effect of EDPs or ELPs on the hMSC differentiation process, the mechanism of action of these peptides has not been elucidated. Therefore, the aim of the present study was to evaluate the impact of the VGVAPG and VVGPGA peptides on the hMSC stemness marker and elucidation of the mechanism of action of these peptides. Our data show that both studied peptides (VGVAPG and VVGPGA) act with the involvement of ERK1/2 and c-SRC kinases. However, their mechanism of activation is probably different in hMSCs derived from adipose tissue. Both studied peptides increase the KI67 protein level in hMSCs, but this is not accompanied with cell proliferation. Moreover, the changes in the NANOG and c-MYC protein expression and in the SOX2 and POU5F1 mRNA expression suggest that EDPs reduced the hMSC stemness properties and could initiate cell differentiation. The initiation of differentiation was evidenced by changes in the expression of AhR and PPARγ protein as well as specific genes (ACTB, TUBB3) and proteins (ß-actin, RhoA) involved in cytoskeleton remodeling. Our data suggest that the presence of EDPs in tissue can initiate hMSC differentiation into more tissue-specific cells.

The role of obesity and adipose tissue dysfunction in osteoarthritis pain.

Obesity has a pivotal and multifaceted role in pain associated with osteoarthritis (OA), extending beyond the mechanistic influence of BMI. It exerts its effects both directly and indirectly through various modifiable risk factors associated with OA-related pain. Adipose tissue dysfunction is highly involved in OA-related pain through local and systemic inflammation, immune dysfunction, and the production of pro-inflammatory cytokines and adipokines. Adipose tissue dysfunction is intricately connected with metabolic syndrome, which independently exerts specific effects on OA-related pain, distinct from its association with BMI. The interplay among obesity, adipose tissue dysfunction and metabolic syndrome influences OA-related pain through diverse pain mechanisms, including nociceptive pain, peripheral sensitization and central sensitization. These complex interactions contribute to the heightened pain experience observed in individuals with OA and obesity. In addition, pain management strategies are less efficient in individuals with obesity. Importantly, therapeutic interventions targeting obesity and metabolic syndrome hold promise in managing OA-related pain. A deeper understanding of the intricate relationship between obesity, metabolic syndrome and OA-related pain is crucial and could have important implications for improving pain management and developing innovative therapeutic options in OA.

Characterization of ibrutinib's effects on the morphology, proliferation, phenotype, viability, and anti-inflammatory potential of adipose-derived mesenchymal stromal cells.

Ibrutinib (IB) is a tyrosine kinase inhibitor (TKI) that has immunomodulatory action and can be used as second-line therapy for steroid-refractory or steroid-resistant chronic Graft versus Host Disease (cGVHD). Mesenchymal stromal cells (MSCs) are distributed throughout the body and their infusion has also been explored as a second-line therapeutic alternative for the treatment of cGVHD. Considering the currently unknown effects of IB on endogenous MSCs, as well as the possible combined use of IB and MSCs for cGVHD, we investigated whether adipose tissue-derived MSCs present IB-targets, as well as the consequences of treating MSCs with this drug, regarding cell viability, proliferation, phenotype, and anti-inflammatory potential. Interestingly, we show for the first time that MSCs express several IB target genes. Also of note, the treatment of such cells with this TKI elevated the levels of CD90 and CD105 surface proteins, as well as VCAM-1. Furthermore, IB-treated MSCs presented increased mRNA expression of the anti-inflammatory genes PD-L1, TSG-6, and IL-10. However, continued exposure to IB, even at low doses, compromised the viability of MSCs. These data indicate that the use of IB can stimulate an anti-inflammatory profile in MSCs, but also that a continued exposure to IB can compromise MSC viability over time.

Red propolis extract associated to platelet-rich plasma and stromal cells with focus in cell therapy and functional tissue regeneration.

The use of platelet-rich plasma (PRP) and adipose-derived stromal cells (ADSC) have been investigated as a form of wound healing enhancement. The objective of this work was to evaluate the association of red propolis (RP) and PRP as inducers of ADSC for application in tissue regeneration. Adipose tissue post-collection and post-cryopreservation was isolated with type II collagenase, characterized by flow cytometry, and differentiated into osteogenic, chondrogenic and adipose cell. The viability of ADSC was evaluated when exposed to different concentrations of RP using the MTT and trypan blue assay. Acridine orange and ethidium bromide (AO/EB) was performed to evaluate cell death events. Horizontal migration methods were investigated in ADSC using autologous and homologous PRP associated with RP (PRP/RP). All assays were processed in triplicate. Flow cytometry and cellular differentiation showed that type II collagenase was effective for isolating ADSC post-collection and post-cryopreservation. RP extracts at concentrations of up to 50 µg.mL-1 presented no cytotoxic effects. Association of PRP and RP at 25 and 50 µg.ml-1 influenced ADSC migration, with total closure on the seventh day after exposition. The results here presented could stimulate proliferation of ADSC cells that may contribute directly or indirectly to the reconstructive process of tissue regeneration.

Correlación del índice de masa corporal y grosor de tejido adiposo en glúteos / Correlation of body mass index and adipose tissue thickness in glutes

Introducción: Con el aumento de la prevalencia de obesidad, se esperaría un mayor espesor glúteo, lo que sería un factor importante en futuras intervenciones en región glútea con fines de optimizar mejores resultados estéticos. Objetivo: Correlacionar el índice de masa corporal y el grosor de tejido adiposo en glúteos en voluntarias que acudieron al Servicio de Cirugía Plástica y Reconstructiva del Hospital Dr. Miguel Pérez Carreño entre enero a marzo, 2023. Métodos: El estudio fue prospectivo, descriptivo y de corte transversal. Se utilizó un sonógrafo Sono Eye 1 para realizar las medidas del glúteo. Mediante una báscula, se midió peso y talla, para posteriormente calcular el IMC, fueron 29 voluntarias de sexo femenino entre 18 a 60 años, sin antecedentes quirúrgicos estéticos previos. Las correlaciones fueron evaluadas con el coeficiente de correlación de Pearson. Se consideró un valor significativo si p < 0,05. Los datos fueron tabulados con STATA 17. Resultados: La edad promedio fue 39 ± 12 años. La mayoría con preobesidad (55,2 %). No hubo diferencias estadísticas en grosor de tejido adiposo, de musculo y espesor de glúteo de acuerdo a la lateralidad; de acuerdo al coeficiente de correlación de Pearson, el IMC no hubo asociación con las medidas combinadas del glúteo izquierdo y derecho del grosor de tejido graso (r = 0,137), grosor muscular (r = 0,115) y espesor glúteo (r = 0,193). Conclusión: Los cambios de las medidas antropométricas de acuerdo al índice de masa corporal, no presentaron correlación estadística con el espesor glúteo. (AU)

Introduction: With the increasing prevalence of obesity, a greater gluteal thickness would be expected, which would be an important factor in future interventions in the gluteal region aimed at optimizing better aesthetic outcomes. Objective: To correlate the body mass index (BMI) and the thickness of adipose tissue in the buttocks of volunteers who attended the Plastic and Reconstructive Surgery Service at Dr. Miguel Pérez Carreño Hospital from January to March, 2023. Methods: The study was prospective, descriptive, and cross-sectional. A Sono Eye 1 sonograph was used to measure the gluteal thickness. Using a scale, weight and height were measured to subsequently calculate the BMI; there were 29 female volunteers aged between 18 and 60 years, without previous aesthetic surgical history. Correlations were assessed using Pearson's correlation coefficient. A significant value was considered if p < 0.05. Data were tabulated using STATA 17. Results: The average age was 39 ± 12 years. The majority had pre-obesity (55,2%). There were no statistical differences in adipose tissue thickness, muscle thickness, and gluteal thickness according to laterality; according to Pearson's correlation coefficient, BMI was not associated with combined measurements of left and right buttock adipose tissue thickness (r = 0,137), muscle thickness (r = 0,115), and gluteal thickness (r = 0,193). Conclusion: Changes in anthropometric measurements according to body mass index did not show a statistical correlation with gluteal thickness. (AU)

Detection of benzotriazole-type ultraviolet stabilizers in sea turtles breeding in the Northwest Pacific Ocean.

Benzotriazole-type ultraviolet stabilizers (BUVSs) are emerging contaminants whose exposure to wildlife is of concern. In this study, we investigated the contamination status of BUVSs in green turtles (Chelonia mydas) breeding at Ogasawara Islands, Japan, through chemical analysis of 10 BUVSs and 26 congeners of polychlorinated biphenyls (PCBs) in adipose tissue (n = 21) and blood plasma (n = 9). BUVSs were detected significant levels in adipose tissue (19 of 21 turtles), and UV-327 (not detected - 14.8 ng/g-lipid, detection frequency: 76 %), UV-326 (not detected - 24.1 ng/g-lipid, 29 %), and UV-328 (not detected - 5.8 ng/g-lipid, 24 %) were frequently detected. Turtles exhibiting sporadically high concentrations of BUVSs (>10 ng/g-lipid) did not necessarily correspond to individuals with high total PCB concentrations (1.03-70.2 ng/g-lipid). The sporadic occurrence pattern of BUVSs suggested that these contaminants in sea turtles cannot be explained solely by diet but are likely derived from plastic debris.

Complications of Fat Grafting and Repositioning for Correction of Lower Eyelid Pouch With Tear Trough Deformity or Lid-Cheek Junction: A Systematic Review.

BACKGROUND: Fat grafting and repositioning may serve as a convenient, economical, and effective surgical method for correcting lower eyelid pouch with a tear trough deformity or lid-cheek junction. However, comprehensive systematic reviews and meta-analyses investigating the complications associated with this technique are lacking. OBJECTIVE: This study aimed to summarize and gather data on complications related to fat grafting and repositioning for the correction of tear trough deformity or lid-cheek junction in lower eyelid blepharoplasty. METHODS: A thorough search was performed across multiple databases including PubMed, Cochrane, Embase, ProQuest, Ovid, Scopus, and Web of Science. Specific inclusion and exclusion criteria were applied to screen the articles. The occurrence of complications was analyzed using a random-effects model. RESULTS: A total of 33 studies involving 4671 patients met the criteria for systematic evaluation and were included in this meta-analysis. The overall complication rates were 0.112 (95% confidence interval [CI]: 0.060-0.177) for total complications, 0.062 (95% CI: 0.003-0.172) for unsatisfactory correction or contour irregularity, 0.062 (95% CI: 0.009-0.151) for hematoma, swelling (not specified as bulbar conjunctiva), ecchymosis, or oozing of blood, and 0.024 (95% CI: 0.013-0.038) for reoperation. CONCLUSIONS: Fat grafting and repositioning for correcting a lower eyelid pouch with tear trough deformity or lid-cheek junction was associated with high rates of complications. Therefore, it is crucial to closely monitor the rates of unsatisfactory correction or contour irregularity, hematoma, swelling (not specified as bulbar conjunctiva), ecchymosis, or oozing of blood, and reoperation. In addition, effective communication with patients should be prioritized.

A RORE-dependent Intronic Enhancer in the IL-7 Receptor-α Locus Controls Glucose Metabolism via Vγ4+ γδT17 Cells.

The IL-7R regulates the homeostasis, activation, and distribution of T cells in peripheral tissues. Although several transcriptional enhancers that regulate IL-7Rα expression in αß T cells have been identified, enhancers active in γδ T cells remain unknown. In this article, we discovered an evolutionarily conserved noncoding sequence (CNS) in intron 2 of the IL-7Rα-chain (IL-7Rα) locus and named this region CNS9. CNS9 contained a conserved retinoic acid receptor-related orphan receptor (ROR)-responsive element (RORE) and exerted RORγt-dependent enhancer activity in vitro. Mice harboring point mutations in the RORE in CNS9 (CNS9-RORmut) showed reduced IL-7Rα expression in IL-17-producing Vγ4+ γδ T cells. In addition, the cell number and IL-17A production of Vγ4+ γδ T cells were reduced in the adipose tissue of CNS9-RORmut mice. Consistent with the reduction in IL-17A, CNS9-RORmut mice exhibited decreased IL-33 expression in the adipose tissue, resulting in fewer regulatory T cells and glucose intolerance. The CNS9-ROR motif was partially responsible for IL-7Rα expression in RORγt+ regulatory T cells, whereas IL-7Rα expression was unaffected in RORγt-expressing Vγ2+ γδ T cells, Th17 cells, type 3 innate lymphoid cells, and invariant NKT cells. Our results indicate that CNS9 is a RORΕ-dependent, Vγ4+ γδ T cell-specific IL-7Rα enhancer that plays a critical role in adipose tissue homeostasis via regulatory T cells, suggesting that the evolutionarily conserved RORΕ in IL-7Rα intron 2 may influence the incidence of type 2 diabetes.

Chromatin Immunoprecipitation in Adipose Tissue and Adipocytes: How to Proceed and Optimize the Protocol for Transcription Factor DNA Binding.

Chromatin immunoprecipitation (ChIP) coupled to qPCR or sequencing is a crucial experiment to determine direct transcriptional regulation under the control of specific transcriptional factors or co-regulators at loci-specific or pan-genomic levels.Here we provide a reliable method for processing ChIP from adipocytes or frozen adipose tissue collection, isolation of nuclei, cross-linking of protein-DNA complexes, chromatin shearing, immunoprecipitation, and DNA purification. We also discuss critical steps for optimizing the experiment to perform a successful ChIP in lipid-rich cells/tissues.

Dietary and circulating branched chain amino acids are unfavorably associated with body fat measures among Chinese adults.

Animal studies showed a detrimental effect of dietary branched chain amino acids (BCAAs) on metabolic health, while epidemiological evidence on dietary BCAAs and obesity is limited and inconclusive. We hypothesized that high dietary and circulating BCAAs are unfavorably associated with obesity in community-dwelling adults. We evaluated the 1-year longitudinal associations of dietary BCAA intake and circulating BCAAs with body fat measures. Body weight, height, and circumferences of the waist (WC) and hip (HC) were measured at baseline and again after 1-year. Body composition and liver fat [indicated by controlled attenuation parameter (CAP)] were also assessed after 1-year. Serum BCAA concentrations at baseline were quantified by liquid chromatography mass spectrometry. Diet was collected using 4 quarterly 3-day recalls during the 1-year. The correlation coefficients between dietary and serum BCAAs were 0.12 (P = .035) for total dietary BCAAs, and ranged from -0.02 (soy foods, P = .749) to 0.18 (poultry, P = .001). Total dietary BCAA intake was associated with increase in body weight (ß = 0.044, P = .022) and body mass index (BMI, ß = 0.047, P = .043). BCAAs from animal foods were associated with increase in HC, while BCAAs from soy foods were associated with weight gain and higher CAP (all P < .05). Serum BCAAs were associated with higher WC, HC, BMI, body fat mass, visceral fat level, and CAP (all P < .05). These results support that dietary and circulating BCAAs are positively associated with the risk of obesity. More cohort studies with validated dietary assessment tools and long-term follow-up among diverse populations are needed to confirm our findings.

Chitosan based extruded nanofibrous bioscaffold for local delivery of mesenchymal stem cells to improve diabetic wound healing.

BACKGROUND: Mesenchymal stem cells (MSCs)-based treatment strategy has shown promise in bolstering the healing process of chronic wounds in diabetic patients, who are at risk of amputation and mortality. To overcome the drawbacks of suboptimal cell retention and diminished cell viability at the injury site, a novel nanofibrous biomaterial-based scaffold was developed by using a controlled extrusion of a polymeric solution to deliver the cells (human adipose-derived MSCs (ADMSCs) and placenta-derived MSCs (PLMSCs)) locally to the animal model of diabetic ulcers. METHODS: The physicochemical and biological properties of the nano-bioscaffold were characterized in terms of microscopic images, FTIR spectroscopy, tensile testing, degradation and swelling tests, contact angle measurements, MTT assay, and cell attachment evaluation. To evaluate the therapeutic efficacy, a study using an excisional wound model was conducted on diabetic rats. RESULTS: The SEM and AFM images of scaffolds revealed a network of uniform nanofibers with narrow diameters between 100-130 nm and surface roughness less than 5 nm, respectively. ADMSCs and PLMSCs had a typical spindle-shaped or fibroblast-like morphology when attached to the scaffold. Desired characteristics in terms of swelling, hydrophilicity, biodegradation rate, and biocompatibility were achieved with the CS70 formulation. The wound healing process was accelerated according to wound closure rate assay upon treatment with MSCs loaded scaffold resulting in increased re-epithelialization, neovascularization, and less inflammatory reaction. Our findings unequivocally demonstrated that the cell-loaded nano-bioscaffold exhibited more efficacy compared with its acellular counterpart. In summation, our study underscores the potential of this innovative cellular scaffold as a viable solution for enhancing the healing of diabetic ulcers. CONCLUSION: The utilization of MSCs in a nanofibrous biomaterial framework demonstrates significant promise, providing a novel avenue for advancing wound care and diabetic ulcer management.

Human adipose and synovial-derived MSCs synergistically attenuate osteoarthritis by promoting chondrocyte autophagy through FoxO1 signaling.

BACKGROUND: Human adipose-derived stem cells (ADSCs) exert a strong anti-inflammatory effect, and synovium-derived stem cells (SDSCs) have high chondrogenic potential. Thus, this study aims to investigate whether a combination of human ADSCs and SDSCs will have a synergistic effect that will increase the chondrogenic potential of osteoarthritis (OA) chondrocytes in vitro and attenuate the cartilage degeneration of early and advanced OA in vitro. METHODS: ADSCs, SDSCs, and chondrocytes were isolated from OA patients who underwent total knee arthroplasty. The ADSCs-SDSCs mixed cell ratios were 1:0 (ADSCs only), 8:2, 5:5 (5A5S), 2:8, and 0:1 (SDSCs only). The chondrogenic potential of the OA chondrocytes was evaluated in vitro with a transwell assay or pellet culture with various mixed cell groups. The mixed cell group with the highest chondrogenic potential was then selected and injected into the knee joints of nude rats of early and advanced OA stages in vivo. The animals were then evaluated 12 and 20 weeks after surgery through gait analysis, von frey test, microcomputed tomography, MRI, and immunohistochemical and histological analyses. Finally, the mechanisms underlying these findings were investigated through the RNA sequencing of tissue samples in vivo and Western blot of the OA chondrocyte autophagy pathway. RESULTS: Among the MSCs treatment groups, 5A5S had the greatest synergistic effect that increased the chondrogenic potential of OA chondrocytes in vitro and inhibited early and advanced OA in vivo. The 5A5S group significantly reduced cartilage degeneration, synovial inflammation, pain sensation, and nerve invasion in subchondral nude rat OA, outperforming both single-cell treatments. The underlying mechanism was the activation of chondrocyte autophagy via the FoxO1 signaling pathway. CONCLUSION: A combination of human ADSCs and SDSCs demonstrated higher potential than a single type of stem cell, demonstrating potential as a novel treatment for OA.

Adipose-derived mesenchymal stem cells suppress fibroblast proliferation of hypertrophic scar through CCL5 and CXCL12.

BACKGROUND AND OBJECTIVE: Adipose-derived mesenchymal stem cells (ADSCs) can accelerate wound healing, reduce scar formation, and inhibit hypertrophic scar (HTS). ADSCs can secrete a large amount of CCL5, and CCL5 has been proved to be pro-inflammatory and pro-fibrotic. CXCL12 (SDF-1) is a key chemokine that promotes stem cell migration and survival. Therefore, this study selected normal skin and HTS conditioned medium to simulate different microenvironments, and analyzed the effects of different microenvironments on the expression of CCL5 and CXCL12 in human ADSCs (hADSCs). MATERIALS AND METHODS: hADSCs with silenced expression of CCL5 and CXCL12 were co-cultured with hypertrophic scar fibroblasts to verify the effects of CCL5 and CXCL12 in hADSCs on the proliferation ability of hypertrophic scar fibroblasts. A mouse model of hypertrophic scar was established to further confirm the effect of CCL5 and CXCL12 in hADSCs on hypertrophic scar formation. RESULTS: CCL5 level was found to be significantly high in hADSCs cultured in HTS conditioned medium. CXCL12 in HTS group was prominently lowly expressed compared with the normal group. Inhibition of CCL5 in hADSCs enhanced the effects of untreated hADSCs on proliferation of HTS fibroblasts while CXCL12 knockdown exerted the opposite function. Inhibition of CCL5 in hADSCs increased the percentage of HTS fibroblasts in the G0/G1 phase while down-regulation of CXCL12 decreased those. Meanwhile, the down-regulated levels of fibroblast markers including collagen I, collagen III, and α-SMA induced by CCL5 knockdown were significantly up-regulated by CXCL12 inhibition. hADSCs alleviate the HTS of mice through CCL5 and CXCL12. CONCLUSION: In summary, our results demonstrated that hADSCs efficiently cured HTS by suppressing proliferation of HTS fibroblasts, which may be related to the inhibition of CXCL12 and elevation of CCL5 in hADSCs, suggesting that hADSCs may provide an alternative therapeutic approach for the treatment of HTS.

Adipose-derived stem cell conditioned medium for hair regeneration therapy in alopecia: a review of literature.

To date, therapeutic choices for alopecia have shown limited effectiveness and safety, making the discovery of new therapeutic choices challenging. Adipose-derived stem cells conditioned-medium (ADSC-CM) contain various growth factors released by ADSCs that may support hair regrowth. This literature review aims to discover the effect and clinical impact of ADSC-CM in the treatment of alopecia. A comprehensive literature search was performed through four databases (Pubmed, ScienceDirect, Cochrane, and Scopus) in September 2021. A combination of search terms including "adipose-derived stem cells" and "alopecia" was used. Studies published in English that included ADSC-CM interventions on alopecia of all types were selected and summarized. A total of five studies were selected for review, all of which were case series. All studies showed a positive outcome for intervention. Outcomes measured in the studies include hair count or hair density, hair thickness, anagen, and telogen hair count. No adverse effects were reported from all studies. Limitations lie in the differences in intervention method, application, and length of treatment. ADSC-CM hair regeneration therapy is an effective and safe treatment for alopecia that may be combined with other types of therapy to improve outcomes.

Establishment of a stem cell administration imaging method in bleomycin-induced pulmonary fibrosis mouse models.

Pulmonary fibrosis is a progressive disease caused by interstitial inflammation. Treatments are extremely scarce; therapeutic drugs and transplantation therapies are not widely available due to cost and a lack of donors, respectively. Recently, there has been a high interest in regenerative medicine and exponential advancements in stem cell-based therapies have occurred. However, a sensitive imaging technique for investigating the in vivo dynamics of transplanted stem cells has not yet been established and the mechanisms of stem cell-based therapy remain largely unexplored. In this study, we administered mouse adipose tissue-derived mesenchymal stem cells (mASCs) labeled with quantum dots (QDs; 8.0 nM) to a mouse model of bleomycin-induced pulmonary fibrosis in an effort to clarify the relationship between in vivo dynamics and therapeutic efficacy. These QD-labeled mASCs were injected into the trachea of C57BL/6 mice seven days after bleomycin administration to induce fibrosis in the lungs. The therapeutic effects and efficacy were evaluated via in vivo/ex vivo imaging, CT imaging, and H&E staining of lung sections. The QD-labeled mASCs remained in the lungs longer and suppressed fibrosis. The 3D imaging results showed that the transplanted cells accumulated in the peripheral and fibrotic regions of the lungs. These results indicate that mASCs may prevent fibrosis. Thus, QD labeling could be a suitable and sensitive imaging technique for evaluating in vivo kinetics in correlation with the efficacy of cell therapy.

Lesson on obesity and anatomy of adipose tissue: new models of study in the era of clinical and translational research.

Obesity is a serious global illness that is frequently associated with metabolic syndrome. Adipocytes are the typical cells of adipose organ, which is composed of at least two different tissues, white and brown adipose tissue. They functionally cooperate, interconverting each other under physiological conditions, but differ in their anatomy, physiology, and endocrine functions. Different cellular models have been proposed to study adipose tissue in vitro. They are also useful for elucidating the mechanisms that are responsible for a pathological condition, such as obesity, and for testing therapeutic strategies. Each cell model has its own characteristics, culture conditions, advantages and disadvantages. The choice of one model rather than another depends on the specific study the researcher is conducting. In recent decades, three-dimensional cultures, such as adipose spheroids, have become very attractive because they more closely resemble the phenotype of freshly isolated cells. The use of such models has developed in parallel with the evolution of translational research, an interdisciplinary branch of the biomedical field, which aims to learn a scientific translational approach to improve human health and longevity. The focus of the present review is on the growing body of data linking the use of new cell models and the spread of translational research. Also, we discuss the possibility, for the future, to employ new three-dimensional adipose tissue cell models to promote the transition from benchside to bedsite and vice versa, allowing translational research to become routine, with the final goal of obtaining clinical benefits in the prevention and treatment of obesity and related disorders.

Improving cardiovascular risk prediction with machine learning: a focus on perivascular adipose tissue characteristics.

BACKGROUND: Timely prevention of major adverse cardiovascular events (MACEs) is imperative for reducing cardiovascular diseases-related mortality. Perivascular adipose tissue (PVAT), the adipose tissue surrounding coronary arteries, has attracted increased amounts of attention. Developing a model for predicting the incidence of MACE utilizing machine learning (ML) integrating clinical and PVAT features may facilitate targeted preventive interventions and improve patient outcomes. METHODS: From January 2017 to December 2019, we analyzed a cohort of 1077 individuals who underwent coronary CT scanning at our facility. Clinical features were collected alongside imaging features, such as coronary artery calcium (CAC) scores and perivascular adipose tissue (PVAT) characteristics. Logistic regression (LR), Framingham Risk Score, and ML algorithms were employed for MACE prediction. RESULTS: We screened seven critical features to improve the practicability of the model. MACE patients tended to be older, smokers, and hypertensive. Imaging biomarkers such as CAC scores and PVAT characteristics differed significantly between patients with and without a 3-year MACE risk in a population that did not exhibit disparities in laboratory results. The ensemble model, which leverages multiple ML algorithms, demonstrated superior predictive performance compared with the other models. Finally, the ensemble model was used for risk stratification prediction to explore its clinical application value. CONCLUSIONS: The developed ensemble model effectively predicted MACE incidence based on clinical and imaging features, highlighting the potential of ML algorithms in cardiovascular risk prediction and personalized medicine. Early identification of high-risk patients may facilitate targeted preventive interventions and improve patient outcomes.

Understanding tissue-resident macrophages unlocks the potential for novel combinatorial strategies in breast cancer.

Tissue-resident macrophages (TRMs) are an integral part of the innate immune system, but their biology is not well understood in the context of cancer. Distinctive resident macrophage populations are identified in different organs in mice using fate mapping studies. They develop from the yolk sac and self-maintain themselves lifelong in specific tissular niches. Similarly, breast-resident macrophages are part of the mammary gland microenvironment. They reside in the breast adipose tissue stroma and close to the ductal epithelium and help in morphogenesis. In breast cancer, TRMs may promote disease progression and metastasis; however, precise mechanisms have not been elucidated. TRMs interact intimately with recruited macrophages, cytotoxic T cells, and other immune cells along with cancer cells, deciding further immunosuppressive or cytotoxic pathways. Moreover, triple-negative breast cancer (TNBC), which is generally associated with poor outcomes, can harbor specific TRM phenotypes. The influence of TRMs on adipose tissue stroma of the mammary gland also contributes to tumor progression. The complex crosstalk between TRMs with T cells, stroma, and breast cancer cells can establish a cascade of downstream events, understanding which can offer new insight for drug discovery and upcoming treatment choices. This review aims to acknowledge the previous research done in this regard while exploring existing research gaps and the future therapeutic potential of TRMs as a combination or single agent in breast cancer.