Cervical foraminal lipoma is a rare cause of cervical radiculopathy. We report the case of a 47-year-old woman who presented with a 1-year history of right arm pain and paresthesia that was refractory to conservative treatment. Magnetic resonance imaging demonstrated a well-defined mass within the right C5-6 neural foramen, causing compression of the exiting C6 nerve root. The patient underwent microsurgical excision via posterior cervical laminoforaminotomy. Intraoperatively, a lipomatous mass compressing the nerve root was identified and completely removed. Histopathological examination confirmed a benign lipoma. Postoperatively, the patient experienced marked symptomatic improvement, with no recurrence of symptoms at a 6-month follow-up. Although it is uncommon, cervical foraminal lipoma should be considered in patients with persistent radiculopathy and atypical imaging findings, and surgical excision can provide favorable clinical outcomes.

Spinal tuberculosis (TB) can be difficult to confirm microbiologically, and delayed treatment may result in irreversible neurological injury. We report the case of a 57-year-old Cambodian man who presented with a 2-month history of upper back pain and right-leg radiculopathy. Thoracic magnetic resonance imaging (MRI) demonstrated destructive spondylitis at T8–9 with epidural and paravertebral abscesses. Despite treatment with broad-spectrum antibiotics and decompression with biopsy at another hospital, serial MRI showed progression of the abscesses and worsening spinal cord compression, followed by bilateral lower-extremity weakness. Repeated acid-fast bacillus staining, mycobacterial culture, TB polymerase chain reaction, and histopathological examination all yielded negative results. A positive QuantiFERON-TB Gold result was considered supportive but not diagnostic evidence because interferon-γ release assays cannot distinguish latent from active TB. Nevertheless, the epidemiological background, MRI findings, chronic inflammatory pathology, and lack of response to non-specific antibiotics supported a clinicoradiological diagnosis of tuberculous spondylitis. Given the patient’s progressive neurological decline, marked destruction of T8 and T9, and overt instability, vertebral column resection was performed at T8–9, followed by anterior reconstruction with a titanium mesh cage and posterior fusion from T5 to T12. Empirical antituberculous chemotherapy was initiated on postoperative day 10. Motor strength improved, inflammatory marker levels decreased, and computed tomography and MRI obtained approximately 3 weeks postoperatively demonstrated stable reconstruction without a drainable fluid collection. This case illustrates that culture-negative spinal TB may require a clinicoradiological diagnosis, early empirical antituberculous therapy, and definitive anterior column reconstruction when progressive instability and neurological compromise are present.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Background and Objectives: Evidence regarding the efficacy and safety of intracardiac echocardiography (ICE) for guidance during transcatheter aortic valve replacement (TAVR) is limited. This study aimed to compare the clinical efficacy and safety of ICE versus transesophageal echocardiography (TEE) for guiding TAVR. Methods: This prospective cohort study included patients who underwent TAVR from August 18, 2015, to June 31, 2021. Eligible patients were stratified by echocardiographic modality (ICE or TEE) and anesthesia mode (monitored anesthesia care [MAC] or general anesthesia [GA]). Primary outcome was the 1-year composite of all-cause mortality, rehospitalization for cardiovascular cause, or stroke, according to the Valve Academic Research Consortium-3 (VARC-3) definition. Propensity score matching was performed, and study outcomes were analyzed for the matched cohorts. Results: Of the 359 eligible patients, 120 patients were matched for the ICE-MAC and TEEGA groups, respectively. The incidence of primary outcome was similar between matched groups (18.3% vs. 20.0%; adjusted hazard ratio, 0.94; 95% confidence interval [CI], 0.53– 1.68; p=0.843). ICE-MAC and TEE-GA also had similar incidences of moderate-to-severe paravalvular regurgitation (PVR) (4.2% vs. 5.0%; adjusted odds ratio, 0.83; 95% CI, 0.23– 2.82; p=0.758), new permanent pacemaker implantation, and VARC-3 types 2–4 bleeding. Conclusions ICE was comparable to TEE for guidance during TAVR for the composite clinical efficacy outcome, with similar incidences of moderate-to-severe PVR, new permanent pacemaker implantation, and major bleeding. These results suggest that ICE could be a safe and effective alternative echocardiographic modality to TEE for guiding TAVR.

Background/Aims: Achieving rapid reduction of low-density lipoprotein cholesterol (LDL-C) levels below 55 mg/dL in patients with acute myocardial infarction (AMI) can be challenging with statins alone. This single-center, retrospective study aimed to assess the impact of single-dose injection of evolocumab 140 mg on LDL-C levels during the peri-percutaneous coronary intervention (PCI) period in patients with AMI. Methods: A total of 95 patients with AMI who underwent PCI were divided into the evolocumab (n = 50) and non-evolocumab (n = 45) groups. Results: The percentage change of LDL-C level at 1–3 weeks from baseline was 78.4 ± 13.4% reduction in the evolocumab group versus 45.6 ± 22.6% in the non-evolocumab group, with a mean difference of -33.5% between the groups (95% CI: -42.6 to -24.5%; p < 0.001). The achievement rate of LDL-C levels below 55 mg/dL at 1–3 weeks was significantly higher in the evolocumab group than in the non-evolocumab group (97.7% vs. 60.0%, p < 0.001). Conclusions Patients with AMI who received single-dose injection of evolocumab 140 mg during the peri-PCI period had a significantly greater LDL-C reduction and higher proportion of patients achieved the target LDL-C level in the early phase AMI than those who did not receive evolocumab.

Various treatment modalities are available for small solitary hepatocellular carcinoma (HCC), yet the optimal primary treatment strategy for tumors ≤ 3 cm remains unclear. This network meta-analysis investigates the comparative efficacy of various interventions on the long-term outcomes of patients with solitary HCC ≤ 3 cm. A systematic search of electronic databases from January 2000 to December 2023 was conducted to identify studies that compared at least two of the following treatments: surgical resection (SR), radiofrequency ablation (RFA), microwave ablation (MWA), and transarterial chemoembolization (TACE). Survival data were extracted, and pooled hazard ratios with 95% confidence intervals were calculated using a frequentist network meta-analysis. A total of 30 studies, comprising 2 randomized controlled trials and 28 retrospective studies, involving 8,053 patients were analyzed. Surgical resection showed the highest overall survival benefit with a p-score of 0.95, followed by RFA at 0.59, MWA at 0.23, and TACE, also at 0.23. Moreover, SR provided the most significant recurrence-free survival advantage, with a p-score of 0.95, followed by RFA at 0.31 and MWA at 0.19. Sensitivity analyses, excluding low-quality or retrospective non-matched studies, corroborated these findings. This network meta-analysis demonstrates that SR is the most effective first-line curative treatment for single HCC ≤ 3 cm, followed by RFA in patients with preserved liver function. The limited data on MWA and TACE underscore the need for further studies.