Infliximab is effective in the treatment of ulcerative colitis with dermatomyositis: A case report.

BACKGROUND: Joint, skin, oral cavity, and eye lesions are the most common extraintestinal manifestations of ulcerative colitis that can occur before or after its onset. The cases of ulcerative colitis with dermatomyositis (DM) are rare. In this study, we report a rare case of ulcerative colitis with DM that was effectively treated with infliximab. CASE SUMMARY: The patient was a 57-year-old female with a 2-year history of DM. The patient was admitted to hospital with abdominal pain, diarrhea, and blood in stool lasting for more than 2 mo. Colonoscopy revealed multiple erosions and ulcers in the entire colon and rectum. Pathological sections showed chronic inflammatory cell infiltration, especially neutrophil infiltration, in the colonic mucosa; therefore, the patient was diagnosed with ulcerative colitis. Preparations of 5-aminosalicylic acid was added to her treatment based on the original treatment for DM, but its effect was unsatisfactory. The patient's discomfort was relieved after infliximab treatment. CONCLUSION: Infliximab can improve DM in the treatment of ulcerative colitis. Specialists need to raise awareness about patients with inflammatory bowel disease who have rare extraintestinal manifestations.

Oxycodone vs Sufentanil in Patient-Controlled Intravenous Analgesia After Gynecological Tumor Operation: A Randomized Double-Blind Clinical Trial.

BACKGROUND: This study aims to compare analgesic effect and side effects of oxycodone and sufentanil in transition analgesia and patient-controlled intravenous analgesia (PCIA) after gynecological tumor operation under general anesthesia. PATIENTS AND METHODS: A prospective, randomized, double-blind research was conducted. Patients undergoing elective gynecological tumor surgery were randomized into four groups: Group S (sufentanil transition analgesia and sufentanil PCIA), Group OS (oxycodone transition analgesia and sufentanil PCIA), Group SO (sufentanil transition analgesia and oxycodone PCIA) and Group O (oxycodone transition analgesia and oxycodone PCIA). The primary outcomes were Numerical Rating Scale (NRS) at rest and coughing, accumulated opioid consumption in PCIA and patients' satisfaction. RESULTS: Patients in Group OS and Group O showed shorter time of consciousness recovery and extubation after surgery. Accumulated opioid consumption in PCIA (equal to morphine) in Group SO and Group O was significantly less than that in Group S and Group OS. Patients in Group O showed lower NRS at rest and coughing, but higher patients' satisfaction 3, 24 and 48 hours after surgery. Patients in Group SO and Group O showed a shorter time of intestinal recovery, first feeding and first-time movement. CONCLUSION: Both oxycodone and sufentanil provided adequate pain relief in transitional analgesia and PCIA treatment after surgery. Oxycodone without background infusion showed less analgesic drug consumption and faster recovery than sufentanil with background infusion in PCIA after gynecological tumor operation under general anesthesia.

Neuroprotective effects of sevoflurane against electromagnetic pulse-induced brain injury through inhibition of neuronal oxidative stress and apoptosis.

Electromagnetic pulse (EMP) causes central nervous system damage and neurobehavioral disorders, and sevoflurane protects the brain from ischemic injury. We investigated the effects of sevoflurane on EMP-induced brain injury. Rats were exposed to EMP and immediately treated with sevoflurane. The protective effects of sevoflurane were assessed by Nissl staining, Fluoro-Jade C staining and electron microscopy. The neurobehavioral effects were assessed using the open-field test and the Morris water maze. Finally, primary cerebral cortical neurons were exposed to EMP and incubated with different concentration of sevoflurane. The cellular viability, lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were assayed. TUNEL staining was performed, and the expression of apoptotic markers was determined. The cerebral cortexes of EMP-exposed rats presented neuronal abnormalities. Sevoflurane alleviated these effects, as well as the learning and memory deficits caused by EMP exposure. In vitro, cell viability was reduced and LDH release was increased after EMP exposure; treatment with sevoflurane ameliorated these effects. Additionally, sevoflurane increased SOD activity, decreased MDA levels and alleviated neuronal apoptosis by regulating the expression of cleaved caspase-3, Bax and Bcl-2. These findings demonstrate that Sevoflurane conferred neuroprotective effects against EMP radiation-induced brain damage by inhibiting neuronal oxidative stress and apoptosis.

The effect of sevoflurane inhalation on gabaergic neurons activation: observation on the GAD67-GFP knock-in mouse.

The mechanisms underlying volatile anesthesia agents are not well elucidated. Emerging researches have focused on the participation of γ-aminobutyric acid (GABA) neurons but there still lacks morphological evidence. To elucidate the possible activation of GABAergic neurons by sevoflurane inhalation in morphology, Fos (as neuronal activity marker) and GABA neurons double labeling were observed on the brain of glutamic acid decarboxylase (GAD) 67-GFP knock-in mice after sevoflurane inhalation. Twenty GAD67-GFP knock-in mice were divided into three groups: S1 group: incomplete anesthesia state induced by sevoflurane; S2 group: complete anesthesia state induced by sevoflurane; control(C) group. Sevoflurane induced a significant increase of Fos expression in the dorsomedial hypothalamic nucleus (DM), periaqueductal grey (PAG), hippocampus (CA1, DG), paraventricular thalamic nucleus (PV), lateral septal nucleus (LS), and cingulate cortex (Cg1 and Cg2) in S1 group compared to C group, and increase of Fos expression in S2 group compared to S1 group. In S2 group, Fos was only expressed in the medial amygdaloid nucleus (MeA), Edinger-Westphal (E-W) nucleus, arcuate hypothalamic nucleus (Arc) and the ventral part of paraventricular hypothalamic nucleus (PaV). Double immunofluroscent staining indicated that in LS, almost all Fos were present in GABAergic neurons. In CA1, DG, DM, cg1, cg2, and PAG, Fos was expressed as well, but only few were present in GABAergic neurons. Fos expression was very high in thalamus, but no coexistence were found as no GABAergic neuron was detected in this area. Our results provided morphological evidence that GABAergic transmission in specific brain areas may participate in the sevoflurane-induced anesthesia.

The effect of ketamine on N-methyl-D-aspartate receptor subunit expression in neonatal rats.

BACKGROUND AND OBJECTIVE: Ketamine has been widely used in paediatric anaesthesia but its influence on development in infants and toddlers still remains unclear. In order to elucidate the influence of ketamine on brain development in neonatal rats, semiquantitative reverse transcriptase PCR, quantitative reverse transcriptase PCR and immunohistochemistry assays were performed to detect the expression of N-methyl-D-aspartate receptor subtypes expression. METHODS: Seven-day-old rats were divided into two random groups. All of them were injected with ketamine intraperitoneally at postnatal day (PND) 7; one group was sacrificed at PND 7, but the other group was sacrificed at PND 28. Each group was divided into five random subgroups. RESULTS: In the semiquantitative reverse transcriptase PCR and quantitative reverse transcriptase PCR experiments, ketamine treatment caused a marked increase in mRNA expression in all subtypes at PND 7 and in NR2A subtypes at PND 28. Immunohistochemistry results indicated that NR2A, 2B and 2C receptor protein increased significantly at PND 7, and NR2A receptor protein increased at PND 28. CONCLUSIONS: Exposure to ketamine resulted in an increase in N-methyl-D-aspartate receptor subunits at PND 7, and this increase persisted to PND 28 in NR2A.