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Background To systematically review the literature and provide a comprehensive understanding of the preemptive effects of oral pregabalin on perioperative pain management in lower limb orthopedic surgery. Method We searched three electronic databases for randomized controlled trials comparing the results of preoperative pregabalin and placebo in patients undergoing lower limb orthopedic surgery. Data analyses were conducted using RevMan 5.4. Results Twenty-one randomized controlled trials met our inclusion criteria. The cumulative opioid consumption within 24 and 48 h postoperatively in the pregabalin group was significantly less than that in the placebo group. The pooled static pain intensity at all time points within the first day was significantly lower in the pregabalin group than in the placebo group. Lower dynamic pain intensity at 48 h was detected in the pregabalin group than in the placebo group. Meanwhile, pregabalin led to a lower incidence of nausea but appeared to be associated with a higher incidence of dizziness and sedation. Subgroup analyses showed that no difference was detected between subgroups stratified by dosing regimen or pregabalin dose in the results of opioid consumption, pain intensity and incidence of complications. Conclusion This meta-analysis supports the use of pregabalin preoperatively in patients undergoing lower limb orthopedic surgery. However, it was wary of the resulting increase in dizziness and sedation. There is no evidence to support the continued use of pregabalin postoperatively or using more than 150 mg of pregabalin per day. Trial registration: This study was registered on 09 November 2021 with INPLASY (registration number: INPLASY2021110031).

Background Hemophagocytic lymphohistiocytosis (HLH) is a rare but potentially life-threatening immune syndrome associated with an excessive systemic inflammatory response. Viral infection caused HLH is the most common secondary HLH, but there are relatively few reports of HLH caused by bacterial infection. The present study is the first case of HLH caused by Streptococcus intermedia meningitis. Case presentation The patient is an 11-year-old and 9-month-old boy. The main symptoms are fever, headache, and vomiting. The imaging finding of the brain is cerebritis and brain abscess. The cerebrospinal fluid (CSF) routine test showed increased nucleated cells, but the smear and culture of CSF were negative. The metagenomics next-generation sequencing (mNGS) of CSF detected Streptococcus intermedius, and the body temperature of the children returned to normal after antibiotic treatment according to etiology. One week later, the child developed fever again, with Kawasaki disease-like manifestations. After high-dose immunoglobulin therapy, the body temperature returned to normal again. The routine blood test showed a progressive decrease in leukocytes and platelets, and bone marrow biopsy detected histiocytes phagocytosed blood cells. Then infection-associated hemophagocytic syndrome (IAHS) was diagnosed, high-dose methylprednisolone and sequential therapy were given and the patient’s recovery was encouraging. Conclusions Our case shows that HLH can also be secondary to Streptococcus intermediate infection, and early bone marrow biopsy is the golden standard for HLH diagnosis. mNGS can improve the detection sensitivity for pathogens when traditional pathogenic tests are negative. Conventional chemotherapy regimens may not be required for IAHS when high-dose glucocorticoids and immunoglobulin therapy are effective.

Astrocytes are present throughout the central nervous system and display complex intracellular Ca 2+ signals. However, it is largely unknown regarding how astrocytic Ca 2+ signals regulate neural microcircuits in developing brain and mammalian behavior in vivo. In this study, we specifically overexpressed the plasma membrane calciumtransporting ATPase2 (PMCA2) of cortical astrocytes and used immunohistochemistry, Ca 2+ imaging, electrophysiology, and behavioral tests to investigate the effects of genetically reducing cortical astrocyte Ca 2+ signaling during a critical developmental period in vivo. We found that reducing cortical astrocyte Ca 2+ signaling during development led to social interaction deficits, depressive-like behaviors, and abnormal synaptic structure and transmission. In addition, restoring cortical astrocyte Ca 2+ signaling using chemogenetic activation of Gq-coupled designer receptors exclusively activated by designer drugs rescued these synaptic and behavioral deficits. Together, our data demonstrate that the integrity of cortical astrocyte Ca 2+ signaling in developing mice is critical for neural circuit development and may be involved in the pathogenesis of developmental neuropsychiatric diseases, such as autism spectrum disorders and depression.