Folia neuropathologica最新文献

Introduction: The aim of the study was to explore the value of serum procalcitonin to albumin (PCT/ALB) and C-reactive protein to albumin (CRP/ALB) ratios in evaluating the condition and prognosis of craniocerebral trauma (CT).

Material and methods: 158 patients with CT admitted to the emergency department of our hospital from January 2020 to June 2022 were selected as the study subjects. According to the Glasgow coma scale (GCS) score, 158 patients with CT were grouped in a mild group (GCS score 13-15 points, n = 68), a moderate group (GCS score 9-12 points, n = 61), and a severe group (GCS score 3-8 points, n = 29). Besides, according to the patient's Glasgow prognosis (GOS) score, 158 patients with CT were divided into a good prognosis group (GOS score 4-5 points, n = 110) and a poor prognosis group (GOS score 1-3 points, n = 48). Serum PCT/ALB and CRP/ALB levels of different groups were compared. The correlation between PCT/ALB and CRP/ALB ratios and the score of GCS and GOS was explored using Pearson correlation analysis. Prognosis-related influencing factors were found out through multivariate logistic regression. The value of serum PCT/ALB and CRP/ALB ratios in evaluating the condition and prognosis of CT was evaluated by the ROC curve.

Results: Patients in the moderate and severe groups had much higher ratios of PCT/ALB and CRP/ALB and sharply lower GCS scores than those in the mild group ( p < 0.001). Compared with the patients in the moderate group, those in the severe group had much higher PCT/ALB and CRP/ALB ratios and obviously lower GCS scores ( p < 0.001). Patients with poor prognosis had markedly higher PCT/ALB and CRP/ALB ratios and memorably lower GOS score than the patients with good prognosis ( p < 0.001). A negative correlation between PCT, CRP, PCT/ALB ratio, CRP/ALB ratio and GCS scores ( r = -0.821, -0.857, -0.750, -0.766, p < 0.001) and GOS scores ( r = -0.636, -0.628, -0.595, -0.628, p < 0.001) was revealed by Pearson correlation analysis. ALB was correlated positively with GCS score and GOS score ( r = 0.381, 0.413, p < 0.001). Multivariate logistic regression analysis exhibited that PCT/ALB ratio and CRP/ALB ratio were related to poor prognosis of CT patients ( p < 0.05). ROC curve analysis showed that the combined PCT/ALB ratio and CRP/ALB area under the curve (AUC) were 0.883 and 0.860, respectively, which were used to assess the severity and predict prognosis of patients with CT.

Conclusions: PCT/ALB and CRP/ALB ratios were positively correlated with the severity and prognosis of patients with CT, and were risk factors for poor prognosis. Early determination of changes in PCT/ALB and CRP/ALB ratios had a certain clinical value for evaluating the condition and prognosis of CT patients.

In recent decades, the production of silver nanoparticles (AgNPs) has shown exponential growth. They are widely used as high-potency antimicrobial agents in a range of medical and consumer products and increasingly in the agricultural sector as a component of plant protection nanoproducts. Due to the risk of environmental hazards, the mechanisms of AgNPs toxicity should be thoroughly investigated to deepen our understanding of the potential negative impact on human health. As oxidative stress (OS) is known to be one of the major mechanisms of AgNP-induced toxicity, in the present study, we have evaluated OS-related changes in cytotoxicity parameters in AgNP-treated cerebellar granule cells (CGCs), as well as the effectiveness of antioxidant defence systems, such as glutathione (GSH), superoxide dismutases (SOD1 and SOD2) and catalase. The results indicate that exposure of CGCs to AgNPs decreases cell viability and mitochondrial potential and increases intracellular calcium concentration and free radical production. The level of intracellular GSH significantly decreases in cells after short-term exposure, but overexpression of SOD1 is observed. In contrast, after long-term exposure, catalase activity is substantially reduced. Supplying extracellular GSH prior to AgNPs significantly improved cell survival and reversed most of the changes in the investigated parameters. This suggests that GSH may be considered as a protective agent suitable for counteracting the negative effects of exposure to AgNPs.

Acrylamide is formed at high temperature during preparation of food rich in carbohydrates. It can be found in animal feed based on potatoes and granulated wheat subjected to thermal treatment. It was demonstrated that acrylamide has a neurotoxic effect in newborn animals in both the central and peripheral nervous system after prenatal exposure to this substance. The aim of the study was to investigate the effect of acrylamide on the immunoreactivity of glial fibrillary acidic protein (GFAP) and S100b in hippocampal astrocytes of weaning rats after oral administration of acrylamide to pregnant mothers at various stages of pregnancy. The dams received acrylamide in drinking water (3 mg/kg b.w.) each day starting on the 6 th day (group II), 11 th day (group III) and 16 th day (group IV) of pregnancy. At 21 postnatal day the pups were euthanized and their brains were dissected. The immunohistochemical reactions for GFAP and S100b protein were performed on the frontal slides containing hippocampus. The obtained results demonstrated a lower density of GFAP-positive cells in rats whose mothers received acrylamide, especially for the longest time. The astrocytes from groups II and III of rats were characterized by a smaller number of processes, which were also shorter in group II. In contrast, the density of S100b-positive cells was significantly higher, especially in the group II animals. Slight alterations may be related to the low dose of acrylamide, short duration of acrylamide administration in groups III and IV, and the possibility of astrocyte regeneration during the period from delivery to weaning, when the studied substance was not administered. The findings suggest potential disruptions in the structural integrity and functional capacity of astrocytes, which are crucial in maintaining the neuronal environment and supporting hippocampal functions.

Oxidative stress is a pivotal stimulating factor in neurocyte apoptosis and has been involved in the pathogenesis of Parkinson's disease (PD). In this study, we have demonstrated that the improvement in the motor disorder of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)/Pro-induced mice caused by b-Ecdysterone (b-Ecd) treatment is due to its antioxidant properties. Using open field, rotarod, and pole climbing tests, we have found that b-Ecd alleviates motor disorder in MPTP/Pro-induced mice and ultimately reduces the impairment of tyrosine hydroxylase (TH)-positive dopaminergic neurons in the substantia nigra (SN). Notably, these effects of b-Ecd were not observed in Nrf2-KO mice. In addition, b-Ecd significantly reduced the formation of ROS and the level of MDA, blocked the increase of LPO, and partially reversed the GSH/GSSG ratio in MPTP/Pro-induced WT mice; however, these results were also not observed in MPTP/Pro-induced Nrf2-KO mice. Mechanistically, b-Ecd enhanced the expression levels of heme oxygenase 1 (HO-1) and GCLc, but not NQO1 (NAD(P)H quinone dehydrogenase 1) and GCLm expression. Interestingly, b-Ecd failed to increase the protein and mRNA levels of HO-1 and GCLc in Nrf2-KO mice, suggesting that b-Ecd attenuates oxidative stress through an Nrf2-dependent mechanism. Furthermore, b-Ecd promoted the expressions of PI3K/Akt phosphorylation (activity) and GSK-3b phosphorylation (inactivity). Conversely, administration of b-Ecd markedly decreased Fyn phosphorylation levels. Collectively, our findings suggest that b-Ecd focuses on Nrf2 in reducing MPTP/Pro-induced oxidative stress and subsequent motor deficits by inhibiting its nuclear export through PI3K/Akt/GSK-3b/Fyn pathway regulation. These further indicate that b-Ecd may be an absorbing therapeutic agent for PD.

Introduction: Traumatic brain injury (TBI) is one of the major causes of death and disability worldwide, and brings a huge burden on the quality of life of patients with TBI and the country's healthcare system. Peripheral organs, especially the kidney, and liver, may be affected by the onset of molecular responses following brain tissue damage. While secondary injury responses post TBI has been well studied in the brain, the effect/consequences of these responses in the peripheral organs have not yet been fully elucidated. Thus, our study aimed to investigate the immunoreactivity of these responses, particularly via proinflammatory cytokines and autophagy markers in the kidney and liver post-acute and chronic TBI.

Material and methods: Mild TBI (mTBI) and repetitive mTBI (r-mTBI) were induced in male and female 2-month-old Balb/c mice via the Marmarou weight-drop model. Liver and kidney tissues were sampled at 24 hours (acute) and 30 days (chronic) post TBI and subjected to histopathological and immunoreactivity analysis.

Results: Interleukin (IL)-6 levels were significantly increased in the male liver and kidney tissues in both TBI groups compared to the control group but were seen to be decreased in the female r-mTBI chronic liver and r-mTBI acute kidney. Tumor necrosis factor a (TNF-a) levels were found to increase only in the female r-mTBI chronic kidney tissue and mTBI chronic liver tissue. IL-1b levels were increased in the male and female r-mTBI liver tissues but decreased in the female mTBI kidney tissue. Inducible nitric oxide synthase (iNOS) levels were found to be significantly increased in the female mTBI acute and r-mTBI chronic kidney tissue and mTBI liver tissue, but decreased in the r-mTBI acute kidney and r-mTBI liver tissues. Beclin-1 levels were increased in male mTBI chronic and r-mTBI acute liver tissue but decreased in the r-mTBI chronic group. LC3A/B and P62/SQSTM1 levels were significantly increased in the female mTBI chronic and male r-mTBI chronic liver tissues but decreased in the male r-mTBI and female r-mTBI acute kidney tissues. Significant histopathological changes were also observed in the liver and kidney tissue which were dependent on the TBI severity, gender, and time post TBI.

Conclusions: The results showed that TBI may elicit peripheral molecular responses, particularly in terms of alteration in the levels of inflammatory cytokines and autophagy markers, which were gender- and time-dependent. This suggests that TBI may have a significant role in the cellular damage of the kidney and liver in both the acute and chronic phases post TBI, thus ensuring that the effects of TBI may not be confined to the brain.

Acute ischemic stroke may present with serious clinical manifestations. Headache attributed to ischemic stroke is one of these clinical manifestations which may be neglected and affect the functional outcome of the patients. Understanding the exact pathophysiology, and recognition of the most clinical and radiological predictors can help to provide good management and open scope for prophylactic approaches. Here, we report a case presented with acute onset of ischemic stroke and developed a new onset headache on the first day of stroke onset. According to the International Classification of Headache Disorders third edition (ICHD-3), the patient has a post-stroke headache. Using transcranial duplex ultrasound, activation of the trigeminovascular pathway could be attributed to the opening of more pain-sensitive collateral channels as the left posterior communicating artery (P Com A). In conclusion, we can predict the development of acute headache at stroke onset based on different clinical and radiological factors. Opening of the collateral channels is strongly implicated in the production of post-stroke headache.

Introduction: First reports associated mutations in triggering receptors expressed on myeloid cells 2 (TREM2) with autosomal recessive Nasu-Hakola disease characterized by painful bone cysts and progressive presenile dementia with psychotic symptoms; however, recent TREM2 biallelic rare variants are suggested to be causative also for the behavioral variant of frontotemporal dementia (bvFTD) without bone involvement.

Material and methods: Clinical data of three unrelated bvFTD patients carrying TREM2 biallelic variants were evaluated. All patients underwent neurological, psychiatric, and cognitive evaluation and neuroimaging. A full neuropsychological assessment was performed in two cases.

Results: Two patients carried compound heterozygous TREM2 variants, p.R62C and p.T66M, and one carried the homozygous p.D87N variant. Based on all obtained clinical and neuroimaging data, a behavioral variant of frontotemporal dementia was diagnosed in all cases. Their clinical manifestation was typical with neuropsychiatric and cognitive features, without bone abnormalities.

Conclusions: Despite all three subjects partially resembling clinical manifestations of Nasu-Hakola disease with TREM2 mutations, we reveal some distinct features, including age of onset, neuroimaging findings, or disease course.