This case report examines the impact of a single session of functional neurology on a 35-year-old female patient diagnosed with lactose intolerance. The patient presented with severe gastrointestinal symptoms, including frequent diarrhea, bloating, and vomiting upon dairy consumption. The intervention aimed to reset dysfunctional neurological programs believed to contribute to her condition. The study utilized a standardized lactose intolerance breath test to measure the hydrogen and methane levels at various intervals before and after treatment. Post-treatment results showed symptomatic relief with the patient reporting normalized bowel movements and the absence of previous symptoms. Despite these improvements, the biochemical markers at higher time points (150 and 175 min) post-treatment remained similar to the pre-treatment values, indicating persistent lactose malabsorption and highlighting the variability of hydrogen measurements. This case report suggests that a single session of functional neurology can significantly alleviate the symptoms of lactose intolerance. However, the preliminary nature of these results underscores the need for further research involving larger sample sizes and long-term follow-up to fully understand the treatment\'s efficacy and underlying mechanisms.

UNASSIGNED: The proportion of Open Pelvic fractures in the paediatric population is relatively high. While operative fixation is the primary approach for managing Open Pelvic fractures in adults, there is limited literature on treatment outcomes in Children, particularly regarding long-term musculoskeletal, neurological, and urogenital function.
UNASSIGNED: This multicentre case series included paediatric patients (<18 years old) with Open Pelvic ring fractures treated at one of two major trauma centres in the Netherlands between January 1, 2001 and December 31, 2021. Data collection involved clinical records and long-term assessments, including musculoskeletal function, growth disorders, urogenital function, sexual dysfunction, and sensory motor function.
UNASSIGNED: A total of 11 patients were included, primarily females (73 %), with a median age at trauma of 12 years (P25-P75 7-14). Most patients had unstable Pelvic ring fractures resulting from high-energy trauma. Surgical interventions were common, with external fixation as the main initial surgical approach (n = 7, 70 %). Complications were observed in eight (73 %) patients. Musculoskeletal function revealed a range of issues in the lower extremity, daily activities, and mental and emotional domain. Long-term radiologic follow-up showed high rates of Pelvic malunion (n = 7, 64 %). Neurological function assessment showed motor and sensory function impairment in a subset of patients. Urogenital function was moderately affected, and sexual dysfunction was limited with most respondents reporting no issues.
UNASSIGNED: Paediatric Open Pelvic fractures are challenging injuries associated with significant short-term complications and long-term musculoskeletal and urogenital issues. Further research is needed to develop tailored treatment strategies and improve outcomes of these patients.

BACKGROUND: A sepsis-like syndrome is known to occur after cardiac arrest, leading to cerebral infiltration by white blood cells (WBC). We hypothesized that pharmacological sequestration of WBC, and more specifically lymphocytes within lymphoid tissues, could reduce the cerebral infiltration by these inflammatory cells and subsequent acute brain injury in a porcine model of cardiac arrest. Lymphocyte sequestration was induced by the sphingosine-1 phosphate receptors agonist fingolimod.
METHODS: In a first set of experiments, anesthetized pigs underwent a sham instrumentation with no cardiac arrest (n = 4). They received an administration of fingolimod (1 mg/kg, i.v.) in order to confirm its effect on WBC. In a second set of experiments, animals randomly received fingolimod or saline two hours prior to an episode of ventricular fibrillation (14 min) with subsequent resuscitation (n = 6 in each group). Neurological injury was assessed 24 h after resuscitation.
RESULTS: In the first set of experiments, WBC and blood lymphocyte counts were significantly reduced by - 61 ± 10% and - 75 ± 6% two hours after fingolimod administration. In the second set of experiments, blood lymphocyte counts, but not WBC, were also significantly reduced after cardiac arrest in Fingolimod vs Control group. However, most cytokine blood levels were not different among groups, including Interleukin (IL)-1ra, IL-8 or IL-18 blood levels. A difference was only observed for IL-6, which decreased in Fingolimod vs Control (e.g., 5.6 ± 4.8 vs 59.4 ± 20.6 pg/ml at 2 h after cardiac arrest, respectively; p = 0.126). Neurofilament light chain (NFL) blood levels were not different among groups (57 ± 25 vs 84 ± 41 pg/ml in Fingolimod vs Control at 6 h after resuscitation, respectively). After awakening, 3 and 2 animals were prematurely euthanized for ethical reasons due to recurrent seizures in Fingolimod and Control groups, respectively. At Day 1, neurological dysfunction score was not different between groups (87 ± 7 vs 87 ± 5% in Fingolimod vs Control, respectively). Conversely, a decrease in the number of CD3 + cells was observed in the brain of surviving animals in Fingolimod vs Control group (3.10 ± 0.50 vs 7.53 ± 0.57 CD3 + cells/field, respectively; p = 0.0286).
CONCLUSIONS: Fingolimod-induced WBC sequestration, and more specifically lymphocytes sequestration, did not improve clinical neurological dysfunction following cardiac arrest although it reduced cerebral infiltration by lymphocytes.

Background Pelvic fractures caused by high-energy trauma, such as motor vehicle accidents or falls from a considerable height, commonly lead to sacral fractures. Approximately a quarter of sacral fractures are linked to neurological injury, and overlooking these fractures may result in neurological issues such as sexual dysfunction, hindered lower limb functionality, and urinary and rectal difficulties. The main goal of this study is to introduce our patient group who underwent either operative or nonoperative treatment for sacral fractures, with a follow-up period of one year, and assess their functional outcomes. Methodology This is a retrospective review of prospectively collected data from a consecutive series of patients at the Apex Trauma Centre, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow. A consecutive series of 24 patients (17-55 years old) with sacral fractures treated either operatively or nonoperatively from 2018 to 2023 was studied. A total of 20 patients were available for follow-up questionnaires, and 20 patients participated in a physical examination. Time to final follow-up averaged 27.19 months (range = 12-57 months). The personal data of each patient was collected, including gender, age, comorbidities, concomitant injuries, mechanism of injury, fracture pattern/classification, surgical or nonsurgical treatment, other surgeries, length of surgery, length of hospital stays, adverse events, complications, neurologic and/or motor deficits, bowel and bladder function, and mortality. At a minimum one-year follow-up, the Majeed score, Oswestry Disability Index (ODI) questionnaire, and Gibbon\'s classification were assessed. Results All fractures were healed. Five patients showed neurological weakness, with three patients having only paresthesia and two patients having lower limb weakness. The mean Majeed score was 75.4, representing a moderate clinical outcome. Final ODI scores averaged 10.6, representing mild disability among patients with sacrum fractures. Overall, 40% of sacrum fractures were associated with sexual dysfunction, with 30% of females and 50% of males reporting this issue. There was no significant difference (p > 0.05) between operated and conservatively managed sacrum fractures concerning ODI scores, neurological deficit, and sexual dysfunction. Conclusions Both male and female patients with traumatic sacrum fractures experienced a significant decrease in their quality of life and sexual function at least 12 months after their surgery. Sacrum fractures are associated with an increased prevalence of sexual dysfunction and bowel/bladder incontinence. Our study findings indicate that patients with sacrum fractures experience similar functional outcomes and incidences of sexual dysfunction irrespective of whether they are managed operatively or conservatively.

[This corrects the article DOI: 10.3389/fmolb.2023.1266243.].

The overconsumption of dietary fructose has been proposed as a major culprit for the rise of many metabolic diseases in recent years, yet the relationship between a high fructose diet and neurological dysfunction remains to be explored. Although fructose metabolism mainly takes place in the liver and intestine, recent studies have shown that a hyperglycemic condition could induce fructose metabolism in the brain. Notably, microglia, which are tissue-resident macrophages (Mφs) that confer innate immunity in the brain, also express fructose transporters (GLUT5) and are capable of utilizing fructose as a carbon fuel. Together, these studies suggest the possibility that a high fructose diet can regulate the activation and inflammatory response of microglia by metabolic reprogramming, thereby altering the susceptibility of developing neurological dysfunction. In this review, the recent advances in the understanding of microglia metabolism and how it supports its functions will be summarized. The results from both in vivo and in vitro studies that have investigated the mechanistic link between fructose-induced metabolic reprogramming of microglia and its function will then be reviewed. Finally, areas of controversies and their associated implications, as well as directions that warrant future research will be highlighted.

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UNASSIGNED: The use of magnesium sulfate for treating aneurysmal subarachnoid hemorrhage (aSAH) has shown inconsistent results across studies. To assess the impact of magnesium sulfate on outcomes after aSAH, we conducted a systematic review and meta-analysis of relevant randomized controlled trials.
UNASSIGNED: PubMed, Embase, and the Cochrane Library were searched for relevant literature on magnesium sulfate for aSAH from database inception to March 20, 2023. The primary outcome was cerebral vasospasm (CV), and secondary outcomes included delayed cerebral ischemia (DCI), secondary cerebral infarction, rebleeding, neurological dysfunction, and mortality.
UNASSIGNED: Of the 558 identified studies, 16 comprising 3,503 patients were eligible and included in the analysis. Compared with control groups (saline or standard treatment), significant differences were reported in outcomes of CV [odds ratio (OR) = 0.61, p = 0.04, 95% confidence interval (CI) (0.37-0.99)], DCI [OR = 0.57, p = 0.01, 95% CI (0.37-0.88)], secondary cerebral infarction [OR = 0.49, p = 0.01, 95% CI (0.27-0.87)] and neurological dysfunction [OR = 0.55, p = 0.04, 95% CI (0.32-0.96)] after magnesium sulfate administration, with no significant differences detected in mortality [OR = 0.92, p = 0.47, 95% CI (0.73-1.15)] and rebleeding [OR = 0.68, p = 0.55, 95% CI (0.19-2.40)] between the two groups.
UNASSIGNED: The superiority of magnesium sulfate over standard treatments for CV, DCI, secondary cerebral infarction, and neurological dysfunction in patients with aSAH was demonstrated. Further randomized trials are warranted to validate these findings with increased sample sizes.

BACKGROUND: Ischemic stroke (IS) occurs when a blood vessel supplying the brain becomes obstructed, resulting in cerebral ischemia. This type of stroke accounts for approximately 87% of all strokes. Globally, IS leads to high mortality and poor prognosis and is associated with neuroinflammation and neuronal apoptosis. D-allose is a bio-substrate of glucose that is widely expressed in many plants. Our previous study showed that D-allose exerted neuroprotective effects against acute cerebral ischemic/reperfusion (I/R) injury by reducing neuroinflammation. Here, we aimed to clarify the beneficial effects D-allose in suppressing IS-induced neuroinflammation damage, cytotoxicity, neuronal apoptosis and neurological deficits and the underlying mechanism in vitro and in vivo.
METHODS: In vivo, an I/R model was induced by middle cerebral artery occlusion and reperfusion (MCAO/R) in C57BL/6 N mice, and D-allose was given by intraperitoneal injection within 5 min after reperfusion. In vitro, mouse hippocampal neuronal cells (HT-22) with oxygen-glucose deprivation and reperfusion (OGD/R) were established as a cell model of IS. Neurological scores, some cytokines, cytotoxicity and apoptosis in the brain and cell lines were measured. Moreover, Gal-3 short hairpin RNAs, lentiviruses and adeno-associated viruses were used to modulate Gal-3 expression in neurons in vitro and in vivo to reveal the molecular mechanism.
RESULTS: D-allose alleviated cytotoxicity, including cell viability, LDH release and apoptosis, in HT-22 cells after OGD/R, which also alleviated brain injury, as indicated by lesion volume, brain edema, neuronal apoptosis, and neurological functional deficits, in a mouse model of I/R. Moreover, D-allose decreased the release of inflammatory factors, such as IL-1β, IL-6 and TNF-α. Furthermore, the expression of Gal-3 was increased by I/R in wild-type mice and HT-22 cells, and this factor further bound to TLR4, as confirmed by three-dimensional structure prediction and Co-IP. Silencing the Gal-3 gene with shRNAs decreased the activation of TLR4 signaling and alleviated IS-induced neuroinflammation, apoptosis and brain injury. Importantly, the loss of Gal-3 enhanced the D-allose-mediated protection against I/R-induced HT-22 cell injury, inflammatory insults and apoptosis, whereas activation of TLR4 by the selective agonist LPS increased the degree of neuronal injury and abolished the protective effects of D-allose.
CONCLUSIONS: In summary, D-allose plays a crucial role in inhibiting inflammation after IS by suppressing Gal-3/TLR4/PI3K/AKT signaling pathway in vitro and in vivo.

Hypoxia induced by high altitude can lead to severe neurological dysfunction. Mitophagy is known to play a crucial role in hypoxic nerve injury. However, the regulatory mechanism of mitophagy during this injury remains unclear. Recent studies have highlighted the role of Sestrin2 (SESN2), an evolutionarily conserved stress-inducible protein against acute hypoxia. Our study demonstrated that hypoxia treatment increased SESN2 expression and activated mitophagy in PC12 cells. Furthermore, the knock-out of Sesn2 gene led to a significant increase in mitochondrial membrane potential and ATP concentrations, which protected the PC12 cells from hypoxic injury. Although the AMPK/mTOR pathway was significantly altered under hypoxia, it does not seem to participate in mitophagy regulation. Instead, our data suggest that the mitophagy receptor FUNDC1 plays a vital role in hypoxia-induced mitophagy. Moreover, SESN2 may function through synergistic regulation with other pathways, such as SESN2/AMPK, to mediate cellular adaptation to hypoxia, including the regulation of mitophagy in neuron cells. Therefore, SESN2 plays a critical role in regulating neural cell response to hypoxia. These findings offer valuable insights into the underlying molecular mechanisms governing the regulation of mitophagy under hypoxia and further highlight the potential of SESN2 as a promising therapeutic target for hypoxic nerve injury.