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1.
Med Sci Monit ; 30: e942574, 2024 Feb 01.
Article in English | MEDLINE | ID: mdl-38297827

ABSTRACT

BACKGROUND Ketamine, a compelling candidate for neuropathic pain management, has attracted interest for its potential to elevate brain-derived neurotrophic factor (BDNF) levels. We aimed to assess the effects of intrathecally administered ketamine on the cerebrospinal fluid (CSF) levels of BDNF(c-BDNF) and allodynia in a rat model of traumatic brain injury (TBI). MATERIAL AND METHODS Forty-five rats were divided into 3 groups: sham operation (Group S), untreated TBI (Group T), and ketamine-treated TBI (Group K), with 15 rats in each group. Rats were anesthetized, and their skulls were secured in a stereotactic frame before undergoing craniotomy. A controlled cortical impact (CCI) was induced, followed by injection of ketamine (3.41 µg/g) into the CSF in Group K. In Group T, no drug was injected after CCI delivery. On postoperative days (POD) 1, 7, and 14, the 50% mechanical withdrawal threshold (50% MWT) and c-BDNF levels were assessed. RESULTS Groups T and K exhibited a significantly lower 50% MWT than Group S on POD 1(6.6 [5.7, 8.7] g, 10.0 [6.8, 11.6] g, and 18.7 [11.6, 18.7] g, respectively; P<0.001). The c-BDNF levels in Group K were significantly higher than those in Groups S and T on POD 1 (18.9 [16.1, 23.0] pg/ml, 7.3 [6.0, 8.8] pg/ml, and 11.0 [10.6, 12.3] pg/ml, respectively; P=0.006). CONCLUSIONS Intrathecal ketamine administration did not exhibit anti-allodynic effects following mild TBI. c-BDNF level is a promising potential indicator for predicting the expression of allodynia after mild TBI.


Subject(s)
Brain Concussion , Ketamine , Rats , Animals , Hyperalgesia/drug therapy , Ketamine/pharmacology , Ketamine/therapeutic use , Brain-Derived Neurotrophic Factor/metabolism , Rats, Sprague-Dawley
2.
Korean J Anesthesiol ; 76(6): 627-639, 2023 12.
Article in English | MEDLINE | ID: mdl-37435613

ABSTRACT

BACKGROUND: We investigated the effects of sevoflurane exposure on the expression of matrix metalloproteinase (MMP), expression and ablation of natural killer group 2, member D (NKG2D) ligands (UL16-binding proteins 1-3 and major histocompatibility complex class I chain-related molecules A/B), and natural killer (NK) cell-mediated cytotoxicity in breast cancer cells. METHODS: Three human breast cancer cell lines (MCF-7, MDA-MB-453, and HCC-70) were incubated with 0 (control), 600 (S6), or 1200 µM (S12) sevoflurane for 4 h. The gene expression of NKG2D ligands and their protein expression on cancer cell surfaces were measured using multiplex polymerase chain reaction (PCR) and flow cytometry, respectively. Protein expression of MMP-1 and -2 and the concentration of soluble NKG2D ligands were analyzed using western blotting and enzyme-linked immunosorbent assays, respectively. RESULTS: Sevoflurane downregulated the mRNA and protein expression of the NKG2D ligand in a dose-dependent manner in MCF-7, MDA-MB-453, and HCC-70 cells but did not affect the expression of MMP-1 or -2 or the concentration of soluble NKG2D ligands in the MCF-7, MDA-MB-453, and HCC-70 cells. Sevoflurane attenuated NK cell-mediated cancer cell lysis in a dose-dependent manner in MCF-7, MDA-MB-453, and HCC-70 cells (P = 0.040, P = 0.040, and P = 0.040, respectively). CONCLUSIONS: Our results demonstrate that sevoflurane exposure attenuates NK cell-mediated cytotoxicity in breast cancer cells in a dose-dependent manner. This could be attributed to a sevoflurane-induced decrease in the transcription of NKG2D ligands rather than sevoflurane-induced changes in MMP expression and their proteolytic activity.


Subject(s)
Breast Neoplasms , Carcinoma, Hepatocellular , Liver Neoplasms , Humans , Female , NK Cell Lectin-Like Receptor Subfamily K/metabolism , Matrix Metalloproteinase 1/metabolism , Sevoflurane , Ligands , Carcinoma, Hepatocellular/metabolism , Liver Neoplasms/metabolism , Killer Cells, Natural/metabolism
3.
Am J Mens Health ; 10(6): 450-458, 2016 11.
Article in English | MEDLINE | ID: mdl-25595018

ABSTRACT

The aim of this research was to compare the health and lifestyle behaviors between male and female nursing professionals. Biological, workplace, and lifestyle factors as well as health behaviors and outcomes are reported as different between male and female nurses. Although male nurses show distinct health-related patterns and experience health disparities at work, few studies have investigated health differences by sex in a large cohort group of nursing professionals. This observation study of Australian and New Zealand nurses and midwives drew data from an eCohort survey. A cohort of 342 females was generated by SPSS randomization (total N=3625), to compare against 342 participating males. Measures for comparison include health markers and behaviors, cognitive well-being, workplace and leisure-time vitality, and functional capacity. Findings suggest that male nurses had a higher BMI, sat for longer, slept for less time, and were more likely to be a smoker than their female nurse counterparts. Men were more likely to report restrictions in bending, bathing, and dressing. In relation to disease, male nurses reported greater rates of respiratory disease and cardiovascular disease, including a three times greater incidence of myocardial infarction, and were more likely to have metabolic problems. In contrast, however, male nurses were more likely to report feeling calm and peaceful with less worries about their health. Important for nurse workforce administrators concerned about the well-being of their staff, the current study reveals significant sex differences and supports the need for gender-sensitive approaches to aid the well-being of male nurses.


Subject(s)
Nurse's Role/psychology , Nurses, Male/statistics & numerical data , Nursing Staff, Hospital/statistics & numerical data , Occupational Health/statistics & numerical data , Adult , Australia , Cohort Studies , Female , Gender Identity , Humans , Job Satisfaction , Male , New Zealand , Nurses, Male/psychology , Nursing Staff, Hospital/psychology , Workplace/psychology , Young Adult
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