The association of androgenetic alopecia with metabolic syndrome has been investigated in several studies, with conflicting results. We conducted a meta-analysis to quantitatively evaluate the risk grade of metabolic syndrome and the metabolic profile in patients with androgenetic alopecia as compared with controls. In total, 19 articles (2,531 participants) satisfied the inclusion criteria. The pooled odds ratio for the prevalence rate of metabolic syndrome between the group with androgenetic alopecia and controls was 3.46 (95% CI: 2.38–5.05; p<0.001). Female sex, early onset, and African ethnicity were associated with an increased risk of metabolic syndrome. Furthermore, patients with androgenetic alopecia had significantly poorer metabolic profiles, such as body mass index, waist circumference, fasting glucose, blood lipids, and blood pressure. It is important for physicians to screen metabolism-related indicators in patients with androgenetic alopecia. More rigorously designed studies and larger sample sizes are required in future studies.

Systemic lupus erythematosus (SLE) is a potentially fatal multisystem inflammatory chronic disorder, the etiology and pathogenesis of which remain unclear. The loss of immune tolerance in SLE patients contributes to the production of autoantibodies that attack multiple organs and tissues, such as the skin, joints, and kidneys. Immune cells play important roles in the occurrence and progression of SLE through amplified immune responses. Sirtuin-1 (SIRT1), an NAD+-dependent histone deacetylase, has been shown to be a pivotal regulator in various physiological processes, including cell differentiation, apoptosis, metabolism, aging, and immune responses, via modulation of different signaling pathways, such as the nuclear factor κ-light-chain-enhancer of activated B cells and activator protein 1 pathways. Recent studies have provided evidence that SIRT1 could be a regulatory element in the immune system, whose altered functions are likely relevant to SLE development. This review aims to illustrate the functions of SIRT1 in different types of immune cells and the potential roles of SIRT1 in the SLE pathogenesis and its therapeutic perspectives.

Background Ultraviolet radiation causes DNA damage in keratinocytes, aggravating cutaneous lupus erythematosus (CLE). High mobility group box 1 (HMGB1) participates in nucleotide excision and may transfer from the nucleus to the cytoplasm in immune active cells and the translocation of HMGB1 may result in DNA repair defects. HMGB1 was observed to transfer from the nucleus to the cytoplasm in the keratinocytes of CLE patients. As a class III histone deacetylases (HDACs), sirtuin-1 (SIRT1) can induce HMGB1 deacetylation. Epigenetic modification of HMGB1 may lead to HMGB1 translocation. Aims We aimed to evaluate the expressions of SIRT1 and HMGB1 in the epidermis of CLE patients and whether decreased SIRT1 leads to HMGB1 translocation through HMGB1 acetylation in keratinocytes. Methods We measured the messenger RNA (mRNA) and protein expressions of SIRT1 and HMGB1 in CLE patients using real-time reverse transcription polymerase chain reaction (RT-qPCR) and western blotting. Keratinocytes were treated with SIRT1 activator resveratrol (Res) and irradiated with ultraviolet B (UVB). We detected the localization expression of HMGB1 by immunofluorescence. The apoptosis level and the cell cycle proportions were measured by flow cytometry. The acetyl-HMGB1 level was detected by immunoprecipitation. Results Compared to healthy controls, the mRNA and protein expressions of SIRT1 in the epidermis of CLE patients were significantly decreased and there was translocation of HMGB1 from the nucleus to the cytoplasm. In keratinocytes, UVB irradiation led to HMGB1 translocation from the nucleus to the cytoplasm. Res treatment inhibited HMGB1 translocation, attenuated the cell apoptosis induced by UVB and decreased the acetyl-HMGB1 level. Limitations We only treated keratinocytes with the SIRT1 activator but did not perform the relevant experiments in keratinocytes with SIRT1 knockdown or overexpression. In addition, the lysine residue site of action of SIRT1 deacetylation of HMGB1 is unclear. The specific mechanism of action of SIRT1 deacetylation of HMGB1 needs to be further investigated. Conclusion SIRT1 may inhibit HMGB1 translocation by HMGB1 deacetylation which inhibited the apoptosis of keratinocytes induced by UVB. Decreased SIRT1 may promote HMGB1 translocation in the keratinocytes of patients with CLE.

The high-performance low-field magnetic resonance imaging (MRI) system, equipped with modern hardware and contemporary imaging capabilities, has garnered interest within the MRI community in recent years. It has also been proven to have unique advantages over high-field MRI in both physical and cost aspects. However, for susceptibility weighted imaging (SWI), the low signal-to-noise ratio and the long echo time inherent at low field hinder the SWI from being applied to clinical applications. This work optimized the imaging protocol to select suitable parameters such as the values of time of echo (TE), repetition time (TR), and the flip angle (FA) of the RF pulse according to the signal simulations for low-field SWI. To improve the signal-to-noise ratio (SNR) performance, averaging multi-echo magnitude images and BM4D phase denoising were proposed. A comparison of the SWI in 0.5T and 1.5T was carried out, demonstrating the capability to identify magnetic susceptibility differences between variable tissues, especially, the blood veins. This would open the possibility to extend SWI applications in the high-performance low field MRI.