Immunoglobulin G4-Related Disease Complicating Ruptured Isolated Iliac Artery Aneurysm: A Complex Management Dilemma.

BACKGROUND Managing IgG4-related disease (IgG4-RD) in the context of vascular complications, such as aneurysms, poses significant challenges, particularly when considering surgical intervention options. The risk of rupture and infection in patients on long-term glucocorticoid therapy complicates treatment decisions. CASE REPORT A 63-year-old woman with a history of IgG4-RD presented with a ruptured right iliac artery aneurysm. She was on long-term oral glucocorticoid therapy. Initial emergency endovascular stent graft implantation was followed by embolization for suspected arterial bleeding and subsequent Salmonella bacteremia. Repeated hospitalizations involved stent graft removal and surgical repair due to persistent infection. Over 2 years, the patient required multiple pelvic drainages and long-term antibiotic and prednisolone therapy, yet her quality of life remained compromised. CONCLUSIONS Our case highlights the unique challenges and considerations in the treatment of IgG4-related aneurysms. Patients with IgG4-RD who are on long-term oral glucocorticoids have an inherent risk of aneurysm rupture. We believe regular follow-ups to monitor the progression of the aorta and iliac arteries into aneurysms are essential. For patients who have developed aneurysms, it is advisable to reduce the dosage of glucocorticoids or even consider surgical treatment as soon as possible. As for the choice of surgical method, there is no consensus yet. While endovascular treatment is less invasive and quicker, it can increase the risk of rupture and bleeding. Open surgery might be a better option. More data are needed to make a definitive judgment.

Assessing Mailuoning injection in wound healing and thrombophlebitis management: A rat model study.

Thrombophlebitis is the inflammatory condition characterized by obstruction of one or more vessels, commonly in the legs, due to the formation of blood clots. It has been reported that traditional Chinese medicine, including Mailuoning injection, is advantageous for treating inflammatory and blood disorders. This research assessed the therapeutic efficacy of Mailuoning injection in the treatment of thrombophlebitis in rodents, as well as investigated its impact on fibrinolysis, inflammation, and coagulation. An experimental setup for thrombophlebitis was established in rodents via modified ligation technique. Five groups comprised the animals: sham operation group, model group, and three Mailuoning treatment groups (low, medium, and high dosages). The pain response, edema, coagulation parameters (PT, APTT, TT, FIB), serum inflammatory markers (IL-6, TNF-α, CRP), and expression levels of endothelial markers (ICAM-1, VCAM-1, NF-κB) were evaluated. Blood flow and vascular function were further assessed by measuring hemorheological parameters and the concentrations of TXB2, ET, and 6-k-PGF1α. In contrast to the sham group, model group demonstrated statistically significant increases in endothelial expression levels, coagulation latencies, and inflammatory markers (p < 0.05). The administration of mailing, specifically at high and medium dosages, resulted in a substantial reduction in inflammatory markers, enhancement of coagulation parameters, suppression of ICAM-1 and VCAM-1 expression, and restoration of hemorheological measurements to baseline (p < 0.05). Significantly higher concentrations of 6-k-PGF1α and lower levels of TXB2 and ET were observed in high-dose group, suggesting that pro- and anti-thrombotic factors were restored to equilibrium. Utilization of Mailuoning injection in rat model of thrombophlebitis exhibited significant therapeutic impact. This effect was manifested through pain alleviation, diminished inflammation, enhanced blood viscosity and facilitation of fibrinolysis. The study indicated that Mailuoning injection may serve as a viable therapeutic option for thrombophlebitis, potentially aiding in the improvement of wound healing by virtue of its anti-inflammatory and blood flow-enhancing characteristics.

Upregulation of the Four and a Half LIM Domains 1 linked with familial venous dysplasia in a familial genetic examination.

BACKGROUND: This study aimed to analyze the mutation site in a family diagnosed with venous dysplasia to identify possible pathogenic genes. METHODS: A 15-year-old female presented with lower extremity venous tortuosity aggravated by ulceration. Only the young sister exhibited similar symptoms within the immediate family of the proband. Whole genome sequencing (WGS) was used to evaluate the mutation sites and chromosome copy number variations (CNV) within the family. The possible pathogenic genes located in the region with CNVs were identified, and the expression of the possible pathogenic genes was verified via quantitative polymerase chain reaction (Q-PCR) and western blotting (WB) analysis. In-vitro models were used to verify the role of possible pathogenic genes linked with the development of venous dysplasia. RESULTS: The high-resolution karyotype analysis of the chromosomes found no abnormalities. The results of the WGS indicated that the proband and her sister shared the CNV events, including a microdeletion on chromosomes X: 13580000-1358555000 and microduplications of chromosome X: 136055000-136290000, chromosome X: 136475000-13671000. The results of the Q-PCR and WB showed that FHL1 was highly expressed in the proband and her sister, indicating that mutations of the FHL1 may have an important role in the development of vein malformations. The results of the in vitro experiments showed that FHL1 overexpression could inhibit venous development. CONCLUSION: The CNV in the Xq26 region (136054501-136288300) was found to be linked with the development of venous malformations in this family. However, further studies are required to evaluate the genetic mechanisms involved in the development of venous malformations.

LIM Homeobox 2 Increases Adhesion-Regulating Molecule 1 Transcription to Facilitate the Pathological Progression of Oxidized Low-Density Lipoprotein-Stimulated Atherosclerotic Cell Models.

Endothelial-mesenchymal transition (EndMT) and endothelial cell apoptosis have been documented to have a role in atherosclerosis (AS) progression. To deepen knowledge in this aspect, our study investigated the effect of LIM homeobox 2 (LHX2) and adhesion-regulating molecule 1 (ADRM1) on EndMT and endothelial cell apoptosis in the oxidized low-density lipoprotein (ox-LDL) -stimulated AS cell model.Ox-LDL was utilized to treat human umbilical vein endothelial cells (HUVECs) for constructing an AS model in vitro, followed by measurement of LHX2 and ADRM1 expressions. Afterward, gain- and loss-of-function assays were performed in HUVECs, followed by detection of cell viability, invasion, migration, and apoptosis and the expression of inflammatory factors [tumor necrosis factor (TNF) -α, interleukin (IL) -1ß, and IL-6], EndMT-related proteins [CD31, vascular epithelium (VE) -cadherin, vimentin, α-smooth muscle actin (SMA), Snai1, Snai2, and Twist1], and the apoptotic protein cleaved caspase-3. Interactions between LHX2 and ADRM1 were analyzed with dual-luciferase reporter gene and chromatin immunoprecipitation assays.High levels of LHX2 and ADRM1 were observed in ox-LDL-induced HUVECs. In ox-LDL-treated HUVECs, LHX2, or ADRM1 knockdown promoted CD31 and VE-cadherin levels, viability, invasion, and migration and reduced apoptosis and the expressions of TNF-α, IL-1ß, IL-6, vimentin, α-SMA, Snai1, Snai2, Twist1, and cleaved caspase-3. Mechanistically, LHX2 bound to the ADRM1 promoter to promote ADRM1 transcription. Overexpression of ADRM1 annulled the aforementioned effects of LHX2 knockdown on ox-LDL-induced HUVECs.LHX2 facilitates the pathological progression of ox-LDL-stimulated AS cell models by increasing ADRM1 transcription.

CircSOD2 Contributes to Tumor Progression, Immune Evasion and Anti-PD-1 Resistance in Hepatocellular Carcinoma by Targeting miR-497-5p/ANXA11 Axis.

Circular RNAs (circRNAs) can function as functional molecules in hepatocellular carcinoma (HCC). Herein, circRNA superoxide dismutase 2 (circSOD2) was researched in HCC progression and immune system. The real-time polymerase chain reaction (qRT-PCR) was used for quantification of circSOD2, microRNA-497-5p (miR-497-5p) and Annexin A11 (ANXA11). Cell assays were performed by 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT) and colony formation assays for proliferation, flow cytometry for apoptosis and cell cycle, wound healing assay for migration and transwell assay for migration/invasion. ANXA11 and metastatic protein levels were measured by western blot. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to analyze target binding. CD8+ T cell immunity was assessed by Immunohistochemistry (IHC) assay, and the effect of circSOD2 on programmed cell death 1 (PD-1) immune checkpoint inhibitors (anti-PD-1) therapy was evaluated by mice xenograft assay. CircSOD2 was upregulated in HCC tissues and cells. Knockdown of circSOD2 resulted in HCC cell growth inhibition, apoptosis promotion, cell cycle arrest and metastasis suppression. Mechanically, circSOD2 promoted HCC development by acting as a miR-497-5p sponge and miR-497-5p played a tumor-inhibitory role in HCC cells by targeting ANXA11. Moreover, circSOD2 induced upregulation of ANXA11 expression by interacting with miR-497-5p. Also, the promoting effects of circSOD2 on immune evasion and anti-PD-1 resistance were related to miR-497-5p/ANXA11 axis. This study elucidated the pivotal function of circSOD2 in HCC progression and immunosuppression by mediating miR-497-6p/ANXA11 axis. CircSOD2/miR-497-5p/ANXA11 axis was a novel view of circRNA research in HCC.

Hepatic portal venous gas complication associated with the thoracic endovascular aortic repair for aortic dissection: a case report and literature review.

Aortic dissection (AD) is a serious disease with a higher mortality. The thoracic endovascular aortic repair (TEVAR) is a first line regimen for aortic dissection. Hepatic portal venous gas (HPVG) is a rare disease, and its definite mechanism is unknown. This is a rare association between the aortic and HPVG. In the present report, we present a case of thoracic aortic dissection, which was the type of Standford B by the computer tomography (CT) angiography, which implicated acute abdominal pain and abdominal distention after TEVAR and immediate abdominal CT shown hepatic portal venous gas (HPVG). The patient, who was treated with conservative treatment of gastrointestinal decompressing, fluid resuscitation, electrolyte replacement, anti-infection, anti-inflammation and anticoagulation, was recovered and discharged without abnormalities. This patient has been followed up for 5 years and has not experienced any physical discomfort related to HPVG. This is the first report that the aortic dissection patient implication with HPVG after thoracic endovascular aortic repair.

Deep Learning Reconstruction Algorithm-Based MRI Image Evaluation of Edaravone in the Treatment of Lower Limb Ischemia-Reperfusion Injury.

This research aimed to evaluate the therapeutic effect of edaravone on lower limb ischemia-reperfusion injury by MRI images of graph patch-based directional curvelet transform (GPBDCT), compression reconstruction algorithm. 200 patients with lower limb ischemia-reperfusion injury after replantation of severed limb were randomly divided into the observation group (edaravone treatment) and control group (Mailuoning injection treatment), with 100 cases in each group. MRI scanning and image processing using the GPBDCT algorithm were used to evaluate the therapeutic effect of the two groups of patients. The results showed that the signal noise ratio (SNR) (22.01), relative l 2 norm error (RLNE) (0.0792), and matching degree γ (0.9997) of the compression and reconstruction algorithm based on GPBDCT were superior to those of the conventional compression and reconstruction algorithm (P < 0.05). MRI examination showed that the decrease of bleeding signal after treatment in the observation group was superior to that in the control group. The levels of superoxide dismutase (SOD) (15 ± 2.02), malondialdehyde (MDA) (2.27 ± 1.02), B cell lymphoma-2 (Bcl-2) (8.5 ± 1.02), Bcl-2-associated X (Bax) (3.7 ± 0.42), and Caspase-3 protein (35.9 ± 5.42) in the observation group before and after treatment were significantly higher than those in the control group (P < 0.05). In conclusion, the GPBDCT-based compression reconstruction algorithm has a better effect on MRI image processing, and edaravone can better remove free radicals and alleviate apoptosis.

Erratum: Rapamycin-induced autophagy activity promotes bone fracture healing in rats.

[This corrects the article DOI: 10.3892/etm.2015.2660.].

Henoch-Schönlein purpura following high-voltage electric burn injury: A case report and review of the literature.

Henoch-Schönlein Purpura (HSP) is a systemic vasculitis of unknown cause, with immune-mediated inflammation of the small vessels, which is characterized by a series of clinical symptoms, such as purpuric rash, colicky abdominal pain, arthritis and acute glomerulonephritis. Twenty-one days following a high-voltage electrical burn injury, a 40-year-old man developed classic clinical symptoms of HSP, including purpuric rash on bilateral lower extremities and abdominal pain. The patient was diagnosed with HSP associated with high-voltage burn injury, which is an extremely rare phenomenon. The diagnosis was based on the clinical manifestations of purpuric rash, abdominal pain and arthralgia, as well as the findings of laboratory examinations [increased levels of serum immunoglobulin A (11.6g/l) and complements C3 (9.6 g/l) and C4 (7.6 g/l), and a positive fecal occult blood test]. The patient was treated with antihistamines (loratadine tablets; 10 mg/day), anti-inflammatory medication (methylprednisolone sodium succinate; 40 mg/day) and oral omeprazole magnesium. The symptoms gradually decreased within 2 weeks from treatment and no abnormality was observed at the 3-, 6- and 12-month follow-ups. In patients who have suffered an electrical burn injury, this autoimmune disease may be caused by long-term inflammation. Therefore, examination of the liver and kidney functions of such patients is important in order to decrease the risk of post-traumatic immune system dysfunction.

Aplasia cutis congenita: A case report and literature review.

Aplasia cutis congenita (ACC) is a rare condition with an unclear pathogenic mechanism, although the condition has been suggested to occur as a result of the disrupted development or degeneration of skin in utero. ACC associated with fetus papyraceus has been described in numerous studies. Although there have been several reports of ACC, surgical treatment of ACC using the head as a site of donor skin is rarely reported. The present study describes the case of a 1-week-old patient with ACC that was healed by skin grafting, using the scalp as the donor site. The outcome of the procedure showed that the use of the scalp as a donor skin site for grafting is an effective treatment for large and deep ACC lesions arising on sites other than the head.

Rapamycin-induced autophagy activity promotes bone fracture healing in rats.

Autophagy is a crucial mediating process for normal bone cell function and metabolism in physiology or pathology. Rapamycin has been demonstrated to induce the autophagy pathway by inhibiting the mammalian target of rapamycin (mTOR) pathway. However, the contribution of autophagy in orthopedic diseases is rarely reported. The aim of the present study was to evaluate the capacity of pharmacologically induced autophagy to modify disease function in a rat model of bone fracture. A femur fracture model was established via surgery in adult male Sprague-Dawley rats. Rapamycin (n=63 rats) or dimethyl sulfoxide (DMSO) vehicle control (n=63 rats) was administered intraperitoneally for 2, 4 and 6 weeks, and 21 randomly selected rats were sacrificed in each group at each time point. X-ray micro-computed tomography and hematoxylin and eosin staining were used to evaluate the extent of fracture healing in each group. The effects of rapamycin on autophagy, mTOR signaling and the expression levels of vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen (PCNA) were analyzed using immunohistochemistry, immunofluorescence staining and western blot analysis. Rapamycin affected the mTOR signaling pathway in rats following fracture, as indicated by the inhibition of the phosphorylation of ribosomal protein S6, a target of mTOR, and activation of microtubule-associated protein 2 light chain 3, a key marker of autophagy. Histomorphometry and image examination indicated that the number of osteoblasts in each section was significantly (P<0.01) increased in the rapamycin group compared with the control group, and this was associated with a significant (P<0.05) increase in mineralized callus fraction. Furthermore, rapamycin treatment increased the expression levels of VEGF and PCNA in the rat callus tissue. These results suggest that rapamycin may serve a beneficial function in fracture healing, and that the underlying mechanism may involve the activation of autophagy.