Effect of perioperative forced air warming blanket on older adult patients undergoing spinal surgery with general anesthesia.

Objective: As the population of patients aged 65 years and older increases, the number of older adult patients undergoing surgery also increases. Older adults are vulnerable to hypothermia due to age-related changes in the thermoregulatory center, which leads to reduced subcutaneous fat tissue, vasomotor response, and heat production. Thus, they are more likely to suffer complications, including cardiovascular changes, blood coagulation disorders, infections, and delayed recovery from surgery. The study investigated the effect of preventive active warming. Methods: This retrospective cohort study conducted at Chungbuk National University Hospital investigated clinical data from older adult patients undergoing spinal surgery from January 1, 2020, to December 13, 2022. In this study, we explored the use of prophylactic active warming during anesthesia induction and post-surgery warming in older adult patients (≥65 years) who experienced hypothermia during and after surgery under general anesthesia. Results: The control group of patients who experienced hypothermia increased from 20% after 10 minutes to 80% after 30 minutes and 100% after 60 minutes. The percentage of patients in the treatment group who initially experienced hypothermia increased from 10% after 30 min to 40% after 60 minutes. However, notably, 90% of these patients had returned to a normal body temperature upon their arrival at the recovery room. The difference in the percentage of patients who developed hypothermia was statistically significant between the two groups. Conclusions: Hypothermia prevention via an air-forced warming blanket was effective for older adult patients undergoing spinal surgery under general anesthesia.

Anesthesia management of deep brain stimulation insertion in a patient with generalized idiopathic dystonia: a case report.

Dystonia is a movement disorder in which excessive muscle contractions cause abnormal movement. It is classified according to its clinical manifestations (onset, distribution, temporal and associated features) and etiology (pathology and inheritance). Deep brain stimulation (DBS) is a surgical procedure used to treat medically intractable dystonia. In this study, we aim to share our experience with general anesthesia in systemic idiopathic dystonia that was not controlled by drugs, along with a literature review. A 21-year-old man with generalized idiopathic dystonia and developmental delay was scheduled to undergo deep brain stimulator implantation under general anesthesia. Intubation of the endotracheal tube and fixation of the stereotactic frame were performed in the intensive care unit (ICU) under sedation and neuromuscular blockade before arrival at the operating room. Total intravenous anesthesia was administered. After an uneventful surgery, the patient was discharged to the ICU with an endotracheal tube. As dystonia has a wide clinical spectrum and DBS requires special anesthetic considerations, anesthesiologists should adopt proper anesthetic depth and neuromuscular blockade according to each patient's condition.

The active metabolite of leflunomide, A77 1726, attenuates inflammatory arthritis in mice with spontaneous arthritis via induction of heme oxygenase-1.

BACKGROUND: Leflunomide is a low-molecular-weight compound that is widely used in the treatment of rheumatoid arthritis. Although leflunomide is thought to act through the inhibition of the de novo pyrimidine synthesis, the molecular mechanism of the drug remains largely unknown. We investigated the antiarthritis effects and mechanisms of action of the active metabolite of leflunomide, A77 1726, in interleukin-1 receptor antagonist-knockout (IL-1Ra-KO) mice. METHODS: 14- to 15-week-old male IL-1Ra-KO mice were treated with 10 or 30 mg/kg A77 1726 via intraperitoneal injection three times per week for 6 weeks. The effects of A77 1726 on arthritis severities were assessed by clinical scoring and histological analysis. The serum concentrations of IL-1ß, tumor necrosis factor-α (TNF-α), and malondialdehyde were measured by enzyme-linked immunosorbent assay. Histologic analysis of the joints was performed using Safranin O, and immunohistochemical staining. The frequencies of interleukin-17-producing CD4+ T (Th17) cells were analyzed by flow cytometry. Heme oxygenase-1 (HO-1) expression in splenic CD4+ T cells isolated from A77 1726-treated arthritis mice were assessed by western blotting. RESULTS: A77 1726 treatment induced heme oxygenase-1 (HO-1) in Jurkat cells and primary mouse T cells. Interestingly, A77 1726 inhibited Th17 cell differentiation. In vivo, A77 1726 reduced the clinical arthritis severity of histological inflammation and cartilage destruction. The joints isolated from A77 1726-treated mice showed decreased expression of inducible nitric oxide synthase, nitrotyrosine, TNF-α, and IL-1ß. The serum levels of TNF-α, IL-1ß, and malondialdehyde were also decreased in A77 1726-treated mice. Whereas the number of Th17 cells in spleens was decreased in A77 1726-treated arthritis mice, a significant increase in the number of Treg cells in spleens was observed. Interestingly, HO-1 expression was significantly higher in splenic CD4+ T cells isolated from A77 1726-treated mice compared with those from vehicle-treated mice, whereas HO-1 expression of splenic non-CD4+ T cells did not differ between groups. CONCLUSION: The inhibitory effects of A77 1726 on joint inflammation and oxidative stress in autoimmune arthritis may be associated with HO-1 induction in CD4+ T cells.

Rebamipide suppresses collagen-induced arthritis through reciprocal regulation of th17/treg cell differentiation and heme oxygenase 1 induction.

OBJECTIVE: Rebamipide, a gastroprotective agent, has the ability to scavenge reactive oxygen radicals. Increased oxidative stress is implicated in the pathogenesis of rheumatoid arthritis (RA). We undertook this study to investigate the impact of rebamipide on the development of arthritis and the pathophysiologic mechanisms by which rebamipide attenuates arthritis severity in a murine model of RA. METHODS: Collagen-induced arthritis (CIA) was induced in DBA/1J mice. Anti-type II collagen antibody titers and interleukin-17 (IL-17) levels were determined using enzyme-linked immunosorbent assay. The expression of transcription factors was analyzed by immunostaining and Western blotting. Frequencies of IL-17-producing CD4+ T cells (Th17 cells) and CD4+CD25+FoxP3+ Treg cells were analyzed by flow cytometry. RESULTS: Rebamipide reduced the clinical arthritis score and severity of histologic inflammation and cartilage destruction in a dose-dependent manner. The joints isolated from rebamipide-treated mice with CIA showed decreased expression of nitrotyrosine, an oxidative stress marker. Rebamipide-treated mice showed lower circulating levels of type II collagen-specific IgG, IgG1, and IgG2a. Whereas the number of Th17 cells in spleens was decreased in rebamipide-treated mice with CIA, a significant increase in the number of Treg cells in spleens was observed. In vitro, rebamipide inhibited Th17 cell differentiation through STAT-3/retinoic acid receptor-related orphan nuclear receptor γt and reciprocally induced Treg cell differentiation through FoxP3. Rebamipide increased Nrf2 nuclear activities in murine CD4+ T cells and LBRM-33 murine T lymphoma cells. Heme oxygenase 1 (HO-1) expression in the spleens was markedly increased in rebamipide-treated mice. CONCLUSION: The inhibitory effects of rebamipide on joint inflammation are associated with recovery from an imbalance between Th17 cells and Treg cells and with activation of an Nrf2/HO-1 antioxidant pathway.

The effect of xylometazoline spray for expansion of nasal cavity.

BACKGROUND: During nasotracheal intubation it is important to have proper pretreatment for nasal mucosa constriction and nasal cavity expanding. Nasal packing of epinephrine gauze is widely used as well as xylometazoline. The aim of this study was to compare and evaluate the efficacy of prophylactic intranasal spray of xylometazoline against epinephrine gauze packing in expanding the nasal cavity. METHODS: Volunteers (n = 32) in their twenties without nasal disease such as septal deviation or rhinitis were enrolled in the study. The more patent nostril in each subject was measured by acoustic rhinometry as the base value. After intranasal spray of xylometazoline, the same nostril was remeasured by same method. Twenty four hours later, intranasal packing of epinephrine gauze was done and the same treatment was done. Subject preferences about the procedures were asked. RESULTS: THERE WERE SIGNIFICANT DIFFERENCE AMONG TREATMENTS (BASE VALUE: 0.582 ± 0.164 cm(2), xylometazoline spray: 0.793 ± 0.165 cm(2), epinephrine gauze packing: 0.990 ± 0.290 cm(2)) in acoustic rhinometry. While the epinephrine gauze packing showed more efficient mucosa constriction, subjects preferred xylometazoline spray. CONCLUSIONS: Even though xylometazoline spray was less effective than epinephrine gauze packing, the simplicity and convenience compensated. In patients undergoing nasotracheal intubation, xylometazoline spray can be an alternative to epinephrine gauze packing.

Changes in the levels of plasma soluble fractalkine in patients with mild cognitive impairment and Alzheimer's disease.

Soluble fractalkine plays a distinctive role in the inflammatory processes of the nervous system; however, the role of soluble fractalkine in Alzheimer's disease (AD) has not yet been investigated. In the present study, we evaluated the levels of plasma soluble fractalkine in patients with mild cognitive impairment (MCI), patients with AD and healthy controls. We also investigated the changes in the levels of plasma soluble fractalkine in patients with AD. A total of 102 patients with cognitive impairment, including 51 patients with MCI, 51 patients with AD, and 57 healthy control subjects, were enrolled in this study. The Mini-Mental Status Examination (MMSE) was used to evaluate the severity of cognitive impairment in patients with MCI and AD. The levels of plasma soluble fractalkine were measured using a specific enzyme-linked immunosorbent assay. There were significant group differences in the levels of plasma soluble fractalkine between the MCI, AD, and control groups. Post hoc analyses revealed significant differences between the MCI and control groups, the AD and control groups, and the MCI and AD groups. The level of plasma soluble fractalkine was significantly greater in the patients with mild to moderate AD than in the patients with severe AD. In addition, there was a positive correlation between MMSE score and plasma soluble fractalkine level in the patients with AD. This study provides preliminary evidence that soluble fractalkine is involved in the pathogenesis of AD.