Silicone implant leakage and capsular calcification are potential complications following breast augmentation with silicone implants. This article presents a case of silicone implant leakage accompanied by capsular calcification following breast augmentation surgery. A 51-year-old female presented with self-reported breast hardening over 21 years after undergoing bilateral silicone implant augmentation mammoplasty and sought medical attention at the Department of Plastic Surgery, the First Affiliated Hospital of Dalian Medical University in 2019. Physical examination revealed eggshell-like hardening of the implants with Baker grade Ⅱ capsular contracture. CT scans demonstrated capsular calcification, leading to bilateral explantation and capsulectomy. Intraoperative findings showed calcified capsules with gelatinous material adherent to the surface. Postoperative compositional analysis confirmed calcium phosphate deposits in the calcified lesions. During the 6-year follow-up, the patient remained asymptomatic without breast pain, new masses, or impaired upper limb mobility. The incisions healed well with no sensory abnormalities. Literature review suggested that implant leakage may result from either long-term mechanical irritation secondary to capsular calcification or occult silicone leakage.

Objective By detecting the changes of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α)in brain tissue,as well as serum S-100β and neuron specific enolases(NSE)in neonatal rats with hypoxic-ischemic encephalopathy(HIE)under differ-ent treatment regimens,the anti-inflammatory and neuroprotective effects of hydrogen gas were explored.Methods HIE animal model was made from 7-day-old newborn SD rats,and then divided into sham operation group,control group,test group 1(saturated hydro-gen saline group),test group 2(mild hypothermia group),and test group 3(combination group)according to completely random number table method.No special treatment was given in the sham operation group,while the control group only had modeling,test group 1 was in-traperitoneally injected with saturated hydrogen saline after modeling,test group 2 was treated with mild hypothermia after modeling,test group3 was treated with mild hypothermia combined with injection of saturated hydrogen saline after modeling.At 1,3 and 7days after modeling,10 rats from each group were decapitated and brain tissue was collected for enzyme-linked immunosorbent assay(ELISA)de-tection of IL-6 and TNF-α,and serum was collected to detect the expression levels of S-100β and NSE.Results The expression levels of IL-6,TNF-α in the brain tissue,S-100β,and NSE in serum of the control group were increased significantly 1day after modeling,began to decline at 3days,and returned to normal at 7days.Compared with the sham operation group,the expression levels of various indicators in the 1day and 3days were statistically significant(P＜0.05).However,the expression levels of various indicators in test group 1and 2decreased compared with the control group on 1day and 3days after modeling(P＜0.05),but were higher than those in test group 3 and sham operation group,with statistical significance(P＜0.05).There was no statistical significance in the comparison of various indicators between test group 1 and 2 at each stage(P＞0.05).Conclusion Hydrogen treatment can reduce the inflammatory response level of the nervous system to some extent,and also has a certain neuroprotective effect on HIE in neonatal rats.

Objective By detecting the changes of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α)in brain tissue,as well as serum S-100β and neuron specific enolases(NSE)in neonatal rats with hypoxic-ischemic encephalopathy(HIE)under differ-ent treatment regimens,the anti-inflammatory and neuroprotective effects of hydrogen gas were explored.Methods HIE animal model was made from 7-day-old newborn SD rats,and then divided into sham operation group,control group,test group 1(saturated hydro-gen saline group),test group 2(mild hypothermia group),and test group 3(combination group)according to completely random number table method.No special treatment was given in the sham operation group,while the control group only had modeling,test group 1 was in-traperitoneally injected with saturated hydrogen saline after modeling,test group 2 was treated with mild hypothermia after modeling,test group3 was treated with mild hypothermia combined with injection of saturated hydrogen saline after modeling.At 1,3 and 7days after modeling,10 rats from each group were decapitated and brain tissue was collected for enzyme-linked immunosorbent assay(ELISA)de-tection of IL-6 and TNF-α,and serum was collected to detect the expression levels of S-100β and NSE.Results The expression levels of IL-6,TNF-α in the brain tissue,S-100β,and NSE in serum of the control group were increased significantly 1day after modeling,began to decline at 3days,and returned to normal at 7days.Compared with the sham operation group,the expression levels of various indicators in the 1day and 3days were statistically significant(P＜0.05).However,the expression levels of various indicators in test group 1and 2decreased compared with the control group on 1day and 3days after modeling(P＜0.05),but were higher than those in test group 3 and sham operation group,with statistical significance(P＜0.05).There was no statistical significance in the comparison of various indicators between test group 1 and 2 at each stage(P＞0.05).Conclusion Hydrogen treatment can reduce the inflammatory response level of the nervous system to some extent,and also has a certain neuroprotective effect on HIE in neonatal rats.

Objective To explore the value of high-frequency ultrasound in the detection of metastatic hepatocellular carcinoma and displaying lesion characteristics. Methods A total of 38 paitients with hepatocellular carcinoma satellite lesions within 40 mm of subcutaneous tissue were underwent low-frequency (1-5 MHz) and high-frequency (6-9 MHz) ultrasound. Detection rates and ultrasonic features were compared. Results High-frequency grayscale ultrasound had a higher detection rate (71.1% vs. 36.8%, P＜0.001). Subgroup analysis showed higher detection rates with chemotherapy history (88.9% vs. 33.3%, P＝0.002), fatty liver (71.9% vs 31.3%, P＜0.001) or superficial lesion (within 20 mm, 76.5% vs 41.2%, P＝0.031). High-frequency ultrasound also showed clearer margins (P＝0.004) and more arterial-phase rim enhancement (P＝0.007). Conclusions 6-9 MHz ultrasound detects metastatic hepatocellular carcinoma, especially superficial lesions, more effectively than 1-5 MHz ultrasound and better visualizes characteristics.

Objective:To study the effects of arsenic exposure on neurological function including voluntary motor ability, anxiety, and short-term memory ability of rats, as well as its impact on the expression levels of synaptic function related genes such as neuropeptide 1 (NLGN1), glutamate receptor 2A (NR2A), and postsynaptic density protein 95 (PSD95).Methods:Forty 3-week-old male specific pathogen free (SPF) grade Wistar rats [weighing (453.97 ± 35.68) g] were selected and divided into four groups using a random number table: 0 (control group) and 2, 10, and 50 mg/L arsenic exposure groups, with 10 rats in each group. They were given deionized water and 2, 10, and 50 mg/L sodium arsenite solutions for 12 weeks, respectively. The open field experiment and Y-maze experiment were used to test the voluntary motor ability, anxiety, and short-term memory ability of rats. Nissl staining was used to observe the pathological damage of the hippocampus in the brain. Real time fluorescence quantitative PCR and Western blot were used to detect the mRNA and protein expression levels of NLGN1, NR2A, and PSD95 in the hippocampus, respectively.Results:The results of the open field experiment revealed that the horizontal movement distances of rats in the 2 and 10 mg/L arsenic exposure groups were reduced compared to the control group, the movement distances in the central area in the 2, 10, and 50 mg/L arsenic exposure groups were reduced compared to the control group, and the residence time in the central area in the 10 and 50 mg/L arsenic exposure groups was reduced compared to the control group ( P < 0.05). The results of Y-maze experiment showed that the retention time of new arms in rats of the 2 and 10 mg/L arsenic exposure groups was shorter than that in the control group ( P < 0.05). The pathological examination results of Nissl staining showed that the control group had abundant Nissl bodies in hippocampal tissues of the cytoplasm with intact neuronal structures, tightly arranged cells, appearing blue purple in color and clear visible nuclei. However, the number of Nissl bodies decreased, intercellular gaps increased, disordered arrangement increased, cytoplasmic staining was lighter, and nuclear shrinkage phenomenon increased in the hippocampal tissues of rats in the 2, 10 and 50 mg/L arsenic exposure groups. The real-time fluorescence quantitative PCR detection results showed that there was a statistically significant difference in the mRNA expression levels of NLGN1, NR2A, and PSD95 in the hippocampal tissues of the four groups ( F = 13.85, 44.94, 4.63, P < 0.05). The results of Western blot analysis showed that the protein expression levels of NLGN1 and NR2A in the hippocampal tissues of rats in the 10 and 50 mg/L arsenic exposure groups were lower than those in the control group (0.65 ± 0.07, 0.69 ± 0.03 vs 1.00 ± 0.04, 0.51 ± 0.11, 0.51 ± 0.13 vs 1.00 ± 0.07, P < 0.05), and the expression level of PSD95 in the hippocampal tissues of rats in the 50 mg/L arsenic exposure group was lower than that in the control group (0.51 ± 0.09 vs 1.00 ± 0.05, P < 0.05). Conclusion:Arsenic may affect synaptic function and cause neurological dysfunction in rats by adjusting the expression levels of NLGN1, NR2A, and PSD95.

Objective To investigate the regulatory role and mechanism of mitochondrial riboso-mal protein S35(MRPS35)in the proliferation,invasion,and migration of colon cancer cells.Meth-ods A total of 120 colon cancer tissues and adjacent normal tissues from patients undergoing radical resection for colon cancer were collected.Human colon cancer cell lines(HCT116,SW480,SW620)and a human normal colon epithelial cell line(NCM460)were cultured.Bioinformatics analysis,real-time quantitative polymerase chain reaction,Western blot,immunohistochemical(IHC)analysis,and cellular functional experiments(plate clone formation assay,scratch test,Transwell migration assay,CCK-8 cell viability assay)were conducted to evaluate the expression and regulatory mechanism of MRPS35 in colon cancer.Results Bioinformatics analysis showed that the expression level of the MRPS35 gene was higher in colorectal cancer tissues than in adjacent normal tissues(P＜0.05).The relative expression levels of MRPS35 mRNA and MRPS35 protein were higher in human colon cancer cell lines(HCT116,SW480,SW620)than in NCM460 cells(P＜0.05).The relative ex-pression level of MRPS35 protein was higher in colon cancer tissues than that in adjacent normal tis-sues(P＜0.05).The expression level of MRPS35 was significantly correlated with tumor diameter,tumor differentiation,and T stage(P=0.002,0.021,0.036).Patients with high MRPS35 expres-sion had a higher overall survival rate than those with low MRPS35 expression(Log-rank P=0.015).After knockdown of MRPS35,the abilities of colon cancer cell cloning,proliferation,invasion,and migration were significantly enhanced.Furthermore,the expression of Wnt1,β-Catenin,and their downstream target proteins increased significantly after MRPS35 knockdown.Conclusion MRPS35 is significantly overexpressed in both colon cancer tissues and colon cancer cells,and it may inhibit the occurrence and development of colon cancer by regulating the Wnt/β-Catenin signaling pathway.Therefore,MRPS35 has the potential to become a novel biomarker and therapeutic target for colon cancer.

Objective:To investigate the association between serum uric acid trajectories and the risk of renal function decline and diabetic kidney disease(DKD) incidence in elderly patients with type 2 diabetes mellitus.Methods:This retrospective cohort study included 5 037 elderly patients with type 2 diabetes mellitus aged 60 years and above who underwent at least three health examinations between 2019 and 2023, with 2019 as the baseline. Latent growth mixture modeling(LGMM) was employed to identify distinct serum uric acid trajectories. Renal function changes and DKD incidence were followed from 2020 to 2023. Binary logistic regression models were used to assess the association between serum uric acid trajectories and the risks of renal function decline and DKD.Results:Two distinct serum uric acid trajectory groups were identified based on model selection criteria: A stable group( n=4 485, 89.04%) and an inverted U-shaped group( n=552, 10.96%). After adjusting for potential confounders, compared with the stable trajectory group, the inverted U-shaped group showed a significantly increased risk of estimated glomerular filtration rate(eGFR) <60 mL·min -1·(1.73 m 2) -1, ≥25% decline in eGFR, doubling of serum creatinine, and DKD events, with OR(95% CI) of 1.99(1.28-3.09), 2.27(1.65-3.13), 1.52(1.09-3.02), and 1.52(1.27-1.82), respectively(all P<0.05). In addition, multivariate analysis indicated that elevated baseline serum uric acid levels were also associated with an increased risk of adverse renal outcomes and DKD incidence; However, the magnitude of the associations was lower than that observed for serum uric acid trajectory groups. Conclusions:An inverted U-shaped serum uric acid trajectory is significantly associated with an increased risk of renal function progression and DKD in elderly patients with type 2 diabetes mellitus. These findings highlight the importance of long-term dynamic monitoring of serum uric acid levels to facilitate early identification and intervention for high-risk individuals.

Objective:To compare the clinical efficacy of laparoscopic Miles surgery through extraperitoneal stoma and intraperitoneal stoma.Methods:The medical records of 140 patients with low rectal cancer after laparoscopic Miles surgery admitted to Gastrointestinal Surgery of Northern Jiangsu People′s Hospital of Jiangsu Province from January 2018 to December 2022 were retrospectively analyzed. Among them, 80 were males and 60 were females, aged 50 to 75 years old, with an average age of 63.95 years old. They were divided into observation group (extraperitoneal stoma, n=70) and control group (intraperitoneal stoma, n=70) based on the stoma method. Through telephone, WeChat, outpatient follow-up and other contact methods, the intraoperative and postoperative recovery, the incidence of perioperative complications (stoma edema, stoma ischemia, peristoma inflammation, perineal/pelvic infection, lung infection) and the incidence of complications at 6 months and 1 year after surgery (stoma stricture, parastoma hernia/internal hernia, stoma prolapse/retraction), and the difference in the ability of artificial anus to control defecation at 1 year after surgery were compared between the two groups. SPSS27.0 statistical software was used for data analysis and processing. Results:(1) Incidence of individual complications such as lung infection between the two groups of patients during the perioperative period (4.3% vs 4.3%, χ2=0.17, P=0.676), stoma edema (25.7% vs 21.4%, χ2=0.36, P=0.550), stoma ischemia (7.1% vs 7.1%, χ2=0.00, P=1.000), peristomal inflammation (20.0% vs. 18.6%, χ2=0.05, P=0.830), perineal/pelvic infection (15.7% vs 27.1%, χ2=2.72, P=0.099), there was no difference between the two groups. There was still no difference in the overall complication rate between the two groups (72.9% vs 78.6%, χ2=0.62, P=0.430). (2) After follow-up to 6 months after surgery, the overall complication rate was 5.7% in the observation group compared with 22.9% in the control group ( χ2=7.06, P=0.008). In particular, the incidence of post-operative parastomal hernia/internal hernia did not occur in the observation group, while 8.6% of patients in the control group occurred (18.6% vs 42.9%, χ2=4.35, P=0.037). (3) After follow-up to 1 year after surgery, the overall complication rate in the observation group was lower than that in the control group ( χ2=8.59, P=0.003). The incidence of parastomal hernia/internal hernia after operation in the observation group was lower than that in the control group (2.9% vs 14.3%, χ2=4.47, P=0.034). (4) At the one-year follow-up, the overall excellent and good rate in the evaluation of bowel function in the observation group was higher than that in the control group (71.4% vs 48.6%, χ2=7.62, P=0.006). Conclusions:In laparoscopic Miles surgery for patients with rectal cancer, choosing extraperitoneal stoma has achieved good results, which can reduce the risk of complications 6 months or even 1 year after surgery, especially in preventing and controlling parastomal hernia/internal hernia. It has significant advantages, and at the same time, it can also promote the recovery of patients′ bowel function and reduce other related complications, thereby ensuring patient safety.

Objective:To explore the effects and potential mechanisms of cell growth regulator 1 ( CGREF1) with an EF hand domain in colorectal cancer proliferation and migration. Methods:Fifty paraffin specimens of colorectal cancer tissues and corresponding paracancerous tissues were selected from January 2023 to January 2024 from the Northern Jiangsu People's Hospital Affiliated to Yangzhou University for analysis, and TCGA, GDSC, KMPLOT and STRING databases were used to explore the expression, prognosis, immune microenvironment, drug sensitivity and related signaling pathway functions of CGREF1 in colorectal cancer. Tissue and cellular expression levels of CGREF1 were analyzed by immunohistochemistry and qRT-PCR. Lentiviral-mediated CGREF1 overexpression in SW-620 cells (OE- CGREF1 vs NC groups) was functionally characterized through CCK-8 proliferation assays, colony formation tests, and scratch wound healing migration assays, with mechanistic investigation via Western blot analysis of apoptosis markers, invasion-related proteins, and RAS/RAF/ERK pathway components. In vivo tumorigenicity was assessed by subcutaneous injection of control or CGREF1-overexpressing SW620 cells in nude mice ( n=3 per group) with tumor growth monitoring. Software of GraphPad Prism 9 was used for statistical analysis of experimental data. Results:CGREF1CGREF1RASERK Studies based on databases, clinical samples and colorectal cancer cell line analyses demonstrated that CGREF1 is downregulated in colorectal cancer, where low CGREF1 expression showed positive correlation with tumor diameter and invasion depth. CGREF1 is closely related to tumor immune infiltration microenvironment and sensitivity to multiple anti-tumor drugs. Overexpression of CGREF1 promoted cell apoptosis while inhibiting cell proliferation, invasion and migration. Overexpression of CGREF1 downregulated the expression levels of RAS, ERK and P-P38/MAPK pathway proteins. CGREF1 inhibited tumor growth in vivo. Conclusion:CGREF1 can inhibit the proliferation, colony formation, and migration of CRC cells through the RAS/ERK/MAPK pathway.

OBJECTIVES: To investigate the role of activating transcription factor 3 (ATF3) in atherosclerotic plaques for regulating inflammatory responses during atherosclerosis (AS) progression. METHODS: Human coronary artery specimens from autopsy cases were examined for ATF3 protein expression and localization using immunofluorescence staining and Western blotting. Apolipoprotein E-deficient (ApoE^-/-) mouse models of AS induced by high-fat diet (HFD) feeding for 12 weeks were subjected to tail vein injection of adeno-associated virus serotype 9 (AAV9) to knock down ATF3 expression. After an additional 5 weeks of HFD feeding, the mice were euthanized for analyzing structural changes of the aortic plaques, and the expression levels of ATF3, inflammatory factors (CD45, CD68, IL-1β, and TNF-α), and NF-κB pathway proteins (P-IKKα/β and P-NF-κB p65) were detected. In the cell experiment, THP-1-derived foam cells were transfected with an ATF3-overexpressing plasmid or an ATF3-specific siRNA to validate the relationship between ATF3 and NF‑κB signaling. RESULTS: In human atherosclerotic plaques, ATF3 expression was significantly elevated and partially co-localized with CD68. ATF3 knockout in ApoE^-/- mice significantly increased aortic plaque volume, upregulated the inflammatory factors, enhanced phosphorylation of the NF‑κB pathway proteins, and increased the expressions of VCAM1, MMP9, and MMP2 in the plaques. In THP-1-derived foam cells, ATF3 silencing caused activation of the NF‑κB pathway, while ATF3 overexpression suppressed the activity of the NF-κB pathway. CONCLUSIONS AS promotes ATF3 expression, and ATF3 deficiency exacerbates AS progression by enhancing plaque inflammation via activating the NF-κB pathway, suggesting the potential of ATF3 as a therapeutic target for AS.
Animals ; Activating Transcription Factor 3/metabolism* ; Signal Transduction ; NF-kappa B/metabolism* ; Humans ; Mice ; Plaque, Atherosclerotic/metabolism* ; Inflammation/metabolism* ; Apolipoproteins E ; Atherosclerosis/metabolism* ; Diet, High-Fat