Clinical characteristics and outcome of primary brain abscess: a retrospective analysis.

BACKGROUND: Patients with primary brain abscess often present with atypical symptoms, and the outcome varies. We investigated the demographic, laboratory, and neuroimaging features of patients with brain abscess at our hospital and identified factors associated with their outcomes. METHODS: We retrospectively collected the data of patients diagnosed with primary brain abscess at our hospital between January 2011 and December 2020. Their clinical characteristics, predisposing factors, laboratory and neuroimaging findings, treatment, and outcome were analyzed. RESULTS: Of the 57 patients diagnosed with primary abscess, 51 (89.47%) were older than 40 years, and 42 (73.68%) were male. Only eight patients (14.04%) showed the classical triad of headache, fever, and focal neurological deficit. Fifteen patients (26.31%) had comorbidities, of which diabetes mellitus was the most common. Positive intracranial purulent material cultures were obtained in 46.15% of the patients, and gram-negative enteric bacteria were found in 33.33% of them, with Klebsiella pneumoniae being the most frequently observed. Surgical treatment, most commonly in the form of stereotactic drainage, was received by 54.39% of the patients. Good outcomes were achieved in 75.44% of the patients. Multivariate logistic regression analysis showed that patients with headaches were more likely to have a poor outcome (odds ratio 6.010, 95% confidence interval 1.114-32.407, p = 0.037). CONCLUSIONS: Male patients and those older than 40 years were more susceptible to brain abscess than female patients and those younger than 40 years, respectively. Only a few patients showed the classical triad of clinical symptoms. Diabetes mellitus was the most common comorbidity. Positive intracranial specimens' culture results were uncommon, with gram-negative enteric bacteria, especially Klebsiella pneumoniae, being the main organisms found. Most patients had a good outcome, and the presence of headache may influence the outcome.

Post-operative cognitive dysfunction in patients following gastrointestinal endoscopic treatment.

We aimed to explore the changes in post-operative cognitive dysfunction (POCD) after gastrointestinal endoscopic treatment using detailed neuropsychological assessments. Patients hospitalized for gastrointestinal endoscopic polypectomy were recruited for neuropsychological evaluations, which included the Chinese version of the Mini-Mental State Examination (MMSE), Auditory-Verbal Learning Test, Digit Span Test (DST), Trail Making Task (TMT), Verbal Fluency Test, Clock Drawing Test, and Stroop test. Cognitive assessments were performed twice: one day before and 24 h after treatment. Healthy control subjects participated in the neuropsychological assessment during the same intervals. Detailed cognitive assessments were performed for 40 patients and 60 control subjects. Based on the Z scores, the incidence of POCD 24 h after gastrointestinal endoscopic treatment was 20%. Patients with POCD had significant impairment in the post-operative MMSE, forward DST, TMT, and Stroop interference effect correct count tests (all p < 0.05). Our preliminary results showed that patients were not fully recovered, and 20% had impairment in multiple cognitive assessments 24 h after a gastrointestinal endoscopy. As attention was affected, safety while discharging those patients should be a concern.

Effect of CPAP on cognitive function in stroke patients with obstructive sleep apnoea: a meta-analysis of randomised controlled trials.

OBJECTIVE: To investigate the effect of continuous positive airway pressure (CPAP) treatment on cognitive function in stroke patients with obstructive sleep apnoea (OSA) by exploring randomised controlled trials (RCTs). METHODS: Published RCTs that assessed the therapeutic effects of CPAP on cognition in stroke patients with OSA, compared with controls or sham CPAP, were included. Electronic databases, including MEDLINE, Embase and Cochrane library, were searched in October 2020 and October 2021. Risk of bias was assessed using the Cochrane collaboration tools. A random effects or fixed effects model was used according to heterogeneity. The outcomes were global cognitive gain, improvement in cognitive domain and subjective sleepiness. RESULTS: 7 RCTs, including 327 participants, comparing CPAP with control or sham CPAP treatment were included. 6 RCTs with 270 participants reported results related to global cognition, and CPAP treatment had no significant effects on global cognitive gain in stroke patients with OSA (standardised mean difference (SMD), 0.18; 95% CI, -0.07 to 0.42; p=0.153). A subgroup analysis showed that an early start to (<2 weeks post stroke) CPAP treatment after stroke significantly improved global cognition (SMD, 0.66; 95% CI, 0.18 to 1.14; p=0.007), which was not found in the case of a delayed start to CPAP treatment. However, CPAP did not significantly help with memory, language, attention or executive function. Moreover, CPAP therapy significantly alleviated subjective sleepiness (SMD, -0.73; 95% CI, -1.15 to -0.32; p≤0.001). CONCLUSIONS: Early initiation of CPAP treatment might contribute to improvement in global cognition in stroke patients with OSA. This study had the following limitations: the sample size in each included study was relatively small; the scales related to cognitive assessment or subjective sleepiness were inconsistent; and the methodological quality was not high. Future trials should focus on including a greater number of stroke patients with OSA undergoing CPAP treatment. PROSPERO REGISTRATION NUMBER: CRD42020214709.

Natural language processing in urology: Automated extraction of clinical information from histopathology reports of uro-oncology procedures.

Objectives: We aimed to automate routine extraction of clinically relevant unstructured information from uro-oncological histopathology reports by applying rule-based and machine learning (ML)/deep learning (DL) methods to develop an oncology focused natural language processing (NLP) algorithm. Methods: Our algorithm employs a combination of a rule-based approach and support vector machines/neural networks (BioBert/Clinical BERT), and is optimised for accuracy. We randomly extracted 5772 uro-oncological histology reports from 2008 to 2018 from electronic health records (EHRs) and split the data into training and validation datasets in an 80:20 ratio. The training dataset was annotated by medical professionals and reviewed by cancer registrars. The validation dataset was annotated by cancer registrars and defined as the gold standard with which the algorithm outcomes were compared. The accuracy of NLP-parsed data was matched against these human annotation results. We defined an accuracy rate of >95% as "acceptable" by professional human extraction, as per our cancer registry definition. Results: There were 11 extraction variables in 268 free-text reports. We achieved an accuracy rate of between 61.2% and 99.0% using our algorithm. Of the 11 data fields, a total of 8 data fields met the acceptable accuracy standard, while another 3 data fields had an accuracy rate between 61.2% and 89.7%. Noticeably, the rule-based approach was shown to be more effective and robust in extracting variables of interest. On the other hand, ML/DL models had poorer predictive performances due to highly imbalanced data distribution and variable writing styles between different reports and data used for domain-specific pre-trained models. Conclusion: We designed an NLP algorithm that can automate clinical information extraction accurately from histopathology reports with an overall average micro accuracy of 93.3%.

Circular RNA lysophosphatidic acid receptor 3 (circ-LPAR3) enhances the cisplatin resistance of ovarian cancer.

Circular RNA (circRNA) is considered to be an important regulator that mediates cancer chemoresistance. But whether circ-LPAR3 is involved in ovarian cancer (OC) cisplatin (DDP) resistance is unclear. The circ-LPAR3, miR-634 and pyruvate dehydrogenase kinase 1 (PDK1) expression was measured by quantitative real-time PCR (qRT-PCR). Cell cisplatin resistance and viability were measured by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide (MTT) assay. In addition, cell colony number, apoptosis, and metastasis were assessed by colony formation assay, flow cytometry and transwell assay. Furthermore, in vivo experiments were performed by constructing mice xenograft models. RNA interaction was confirmed by dual-luciferase reporter assay, and PDK1 protein expression was examined by Western blot analysis. Our results showed that circ-LPAR3 was markedly upregulated in DDP-resistant OC tissues and cells. Silencing of circ-LPAR3 enhanced the DDP sensitivity of OC cells and tumors. MiR-634 could interact with circ-LPAR3, and its inhibitor overturned the regulation of si-circ-LPAR3 on cell DDP resistance. Additionally, PDK1 was targeted by miR-634, and its overexpression inverted the effect of miR-634 on cell DDP resistance. To sum up, circ-LPAR3 might contribute to the DDP resistance of OC via the miR-634/PDK1 axis.

[Effects of Butylphthalide on the expressions of HMGB1 and RAGE in frontal lobe of rats after chronic sleep deprivation].

OBJECTIVE: To investigate the effects of Butylphthalide on the expressions of HMGB1 and RAGE in frontal lobe of rats after chronic sleep deprivation. METHODS: Chronic sleep deprivation and butylphthalide treatment was performed in Sprague Dawley(SD)rats and the rats were divided into three groups (n＝6): platform control group, chronic sleep deprivation group and chronic sleep deprivation + butylphthalide intervention group. Rats suffering chronic sleep deprivation were put in multiple platforms box for 18 h per day and sleep deprivation lasted for 28 days. Rats in butylphthalide intervention group were intraperitoneally injected with butylphthalide 100 mg/(kg·d) for 14 days after sleep deprivation. After collecting brains, high-mobility group box (HMGB1) and nuclear transcription factor kappB (NF-κB)p65 were detected by immunohistochemistry. The expression of HMGB1, silent information regulator of transcription 1 (SIRT1), receptor for advanced glycation end-products (RAGE) and NF-κB in frontal lobe were determinated by Western blot. RESULTS: Compared with platform control group, the expression levels of HMGB1, RAGE and nuclear NF-κB p65 were increased significantly, while the expression of SIRT1 was decreased siginificantly in frontal lobe of chronic sleep deprivation group (all P＜0.05). Compared with chronic sleep deprivation group, the expression levels of of HMGB1, RAGE and nuclear NF-κB p65 were decreased significantly, while the expression of SIRT1 was increased significantly in chronic sleep deprivation + butylphthalide intervention group (all P＜0.05). CONCLUSION: Butylphthalide can inhibit HMGB1/RAGE/NF-κB pathway in frontal lobe of rats after chronic sleep deprivation by changing the expression of HMGB1 and RAGE, and reducing the nuclear translocation of NF-κBp65.

Predictive models based on machine learning for bone metastasis in patients with diagnosed colorectal cancer.

Background: This study aimed to develop an artificial intelligence predictive model for predicting the probability of developing BM in CRC patients. Methods: From SEER database, 50,566 CRC patients were identified between January 2015 and December 2019 without missing data. SVM and LR models were trained and tested on the dataset. Accuracy, area under the curve (AUC), and IDI were used to evaluate and compare the models. Results: For bone metastases in the entire cohort, SVM model with poly as kernel function presents the best performance, whose accuracy is 0.908, recall is 0.838, and AUC is 0.926, outperforming LR model. The top three most important factors affecting the model's prediction of BM include extraosseous metastases (EM), CEA, and size. Conclusion: Our study developed an SVM model with poly as kernel function for predicting BM in CRC patients. SVM model could improve personalized clinical decision-making, help rationalize the bone metastasis screening process, and reduce the burden on healthcare systems and patients.

Enriched Environment Decreases Cognitive Impairment in Elderly Rats With Prenatal Mobile Phone Exposure.

Mobile phone use has rapidly increased worldwide, and pregnant women are passively or actively exposed to the associated electromagnetic radiation. Maternal cell phone exposure is related to behavioral difficulties in young offspring. However, whether prenatal mobile phone exposure can predispose the elderly offspring to cognitive impairment is unclear. The enriched environment (EE) has shown positive effects on cognition in an immature brain, but its impact on aging offspring after prenatal cell phone exposure is unknown. This study aimed to investigate whether prenatal exposure to mobile phone exerts long-term effects on cognition in elderly rat offspring and whether EE during adulthood can rescue cognitive impairment by altering the synaptic plasticity. Pregnant rats were subjected to prenatal short-term or long-term cell phone exposure and offspring rats were randomly assigned to standard or EE. Spatial learning and memory were investigated using Morris water maze (MWM) in elderly rat offspring. Hippocampal cellular morphology was assessed by hematoxylin-eosin staining and synaptic ultrastructure was evaluated with transmission electron microscopy. Expression of synaptophysin (SYN), postsynaptic density-95 (PSD-95), and brain-derived neurotrophic factor (BDNF) were detected by western blot. The results demonstrated that prenatal long-term but not short-term exposure to mobile phone lead to cognitive impairment, morphological changes in the hippocampal cells, reduced synaptic number, decreased SYN, PSD-95, and BDNF expression in elderly offspring, which were alleviated by postnatal EE housing. These findings suggest that prenatal long-term mobile phone exposure may pose life-long adverse effects on elderly offspring and impair cognition by disrupting the synaptic plasticity, which may be reversed by postnatal EE housing.

[Effects of butylphthalide on microglia activation in frontal lobe of rats after chronic sleep deprivation].

Objective: To evaluate the effects of butylphthalide on microglia activation and inflammatory factors in frontal lobe of rats after chronic sleep deprivation. Methods: Rats were divided into four groups(n＝8): control group, platform group, chronic sleep deprivation group and butylphthalide intervention group. Chronic sleep deprivation was performed in rats of chronic sleep deprivation group and butylphthalide intervention group for 18 h per day using the multiple platforms method, and sleep deprivation lasted for 28 days. At the same time, rats in platform group were put in platform, while rats in control group were in normal sleep. After 28 days of sleep deprivation, rats in butylphthalide intervention group were intraperitoneally injected with butylphthalide 100 mg/kg for 14 days, meanwhile rats in other groups were intraperitoneally injected with saline. Then brains were collected and ionized calcium binding adaptor molecule-1 (Iba-1) positive cells in cortex in frontal lobe were studied and counted. The expressions of inducible nitric oxide synthase (iNOS) and arginase1 (Arg1) in frontal lobe were detected by Western blot, and the mRNA levels of interleukin-1 (IL-1), IL-6, tumor necrosis factor-α (TNF-α) were determined by real-time PCR. Results: Compared with control or platform group, the Iba-1 positive cells in chronic sleep deprivation group were large with long process, and increased cell counts were also found in the chronic sleep deprivation group (all P＜0. 05). Moreover, the mRNA expression levels of iNOS, IL-1, IL-6, TNF-α were increased, while the expression of Arg1 was decreased in frontal lobe in rats of the chronic sleep deprivation group compared with the control or platform group (all P＜0. 05). The Iba-1 positive cells in butylphthalide intervention group were reduced compared with chronic sleep deprivation group (P＜0. 05). And the mRNA expression levels of iNOS, IL-1, IL-6 and TNF-α were decreased, while the expression of Arg1 did not chang in rats of the butylphthalide intervention group compared with the chronic sleep deprivation group (all P＜0. 05). Conclusion: Butylphthalide might inhibit the activation and decrease the inflammatory factors in frontal lobe of rats after chronic sleep deprivation.

[The effects of prenatal radiation of mobile phones on white matter in cerebellum of rat offspring].

OBJECTIVE: To evaluate the effects of prenatal radiation of 850～1 900 MHz mobile phone on white matter in cerebellum of adult rat offspring. METHODS: Pregnant rats were randomly divided into short term maternal radiation group, long term maternal radiation group and control group. Rats in short term and long term maternal radiation group were exposed to 6 h/d and 24 h/d mobile phone radiation during 1-17 days of pregnancy, respectively. The cerebellums of offspring rats at the age of 3 month(n＝8)were taken. Cell morphology in cerebellum was studied by hematoxylin-eosin (HE) staining. The expressions of myelin basic protein (MBP), neurofilament-L (NF-L) and glial fibrillary acidic protein (GFAP) in cerebellum of rat offspring were detected by immunohistochemistry and Western blot. RESULTS: Compared to control group, the morphological changes of purkinje cells in cerebellum were obvious in rat offspring of short term and long term maternal radiation group. Compared to control group, decreased MBP and NF-L expressions and increased GFAP expression were observed in long term maternal radiation group(all P＜0.05). Compared to short term radiation group, the expressions of MBP and NF-L were down-regulated (all P＜0.05) and the expression of GFAP was up- regulated(P＜0.05) in long term radiation group. CONCLUSION: Prenatal mobile phone radiation might lead to the damage of myelin and axon with activity of astrocytes in cerebellum of male rat offspring, which is related to the extent of radiation.

Rhabdomyolysis following status epilepticus with hyperuricemia: A case report and literature review.

RATIONALE: Rhabdomyolysis owing to status epilepticus (SE) can be life-threating, with acute kidney injury (AKI) the most serious complication; therefore, early recognition of the risk factors is important. Hyperuricemia after epileptic seizures has been reported, and severe hyperuricemia can lead to acute renal function damage. PATIENT CONCERNS: We present the case of a 21-year-old man hospitalized for SE, who had especially high level of blood uric acid (UA) at initial presentation. DIAGNOSIS: The patient was diagnosed with rhabdomyolysis due to SE. INTERVENTIONS: The patient was treated with hydration and bicarbonate therapy. But he developed acute kidney failure (AKF) and hemodialysis was performed. OUTCOMES: After hemodialysis, his symptoms disappeared and laboratory data returned to normal. LESSONS: Hyperuricemia after SE might indicate severe muscle damage or reduced clearance of metabolites, and could be a risk factor for kidney dysfunction, especially with rhabdomyolysis. To our knowledge, this is the first report of rhabdomyolysis following SE with hyperuricemia.

[cts of prenatal exposure of 850-1900MHz mobile phone on the expression of PCNA and DCX in dentate gyrus of offspring rats].

OBJECTIVE: To evaluate the effect of prenatal mobile phone exposure on the expression of proliferating cell nuclear antigen (PCNA) and doublecortin (DCX) in dentate gyrus of offspring rats. METHODS: The rat model of prenatal mobile phone exposure was established and there were three groups including control group, short term maternal exposure group and long term maternal exposure group(n=6). From pregnant day 1 to day 17, pregnant rats in long term and short term maternal exposure group were exposed to an mobile phone in talking mode for 6 h/d and 24 h/d, respectively. Length of pregnancy, maternal body weight gain, litter size and pup's body weight were observed. The cell morphology in dentate gyrus of offspring rats at the age of 1 month was studied by cresyl violet staining. The immunohistochemical expression of PCNA and DCX in dentate gyrus of rat offspring were detected, and the expression of DCX and brain derived neurotrophic factor (BDNF) in hippocampus of rat offspring were evaluated by Western blot. RESULTS: There was no difference in length of pregnancy, maternal body weight gain, litter size and pup's body weight among three groups. The morphological changes of pyramidal cells in the polymorphic layer and DCX-positive cells in the dentate gyrus were obvious in rat offspring of long term maternal exposure group. There were less PCNA-positive cells in dentate gyrus and decreased expression of DCX and BDNF in hippocampus by Western blot in long term maternal exposure group compared with control and short term maternal exposure group (all P<0.05). CONCLUSIONS: Long term prenatal mobile phone exposure might inhibit the expression of PCNA and DCX in dentate gyrus of rat offspring by down-regulating BDNF.

Automating the Renal Cell Carcinoma Registry in Singapore: A Case Study on the Integration of the Research Electronic Data Capture System with the Enterprise Data Warehouse.

The renal cell carcinoma registry (RCCR) at the Singapore General Hospital was established in the 1980s. In 2012, the registry transited to a partially automated system using Research Electronic Data Capture (REDCap) and Oracle Business Intelligence Enterprise Edition (OBIEE), which is a platform for retrieval of electronic data from the Electronic Health Intelligence System (eHIntS). A committee was formed of experts from the department of urology and the health services research center, as well as an information technology (IT) team to evaluate the efficacy of the partially automated system. In the 5 years after the new system was implemented, 1,751 cases were recorded in the RCCR. The casefinding completeness increased by 1.9%, the data accuracy rate was 97%, and the efficiency increased by 12%. Strengths of the new system after partial automation were: (1) secure access to the registry via the hospital Web, (2) direct access to REDCap via the electronic medical records system, (3) automated and timely data extraction, and (4) visual presentation of data. On the other hand, we also encountered several challenges in the process of automating the registry, including limited IT support, limited expertise in matching data variables from RCCR and eHIntS, and limited availability and accessibility of eHIntS information for import into REDCap. In summary, despite these challenges, partial automation was achieved with the REDCap/OBIEE system, enhancing efficiency, data security, and data quality.

Maternal hypoxia increases hippocampal cell susceptibility to ischemia after middle cerebral artery occlusion in rat offspring.

Introduction: Maternal hypoxia induces an adverse uterine environment and may induce long-term effects in offspring. This study investigated whether maternal hypoxia increases hippocampal cell vulnerability and exacerbates neurological impairments in adult rat offspring following ischemia. Material and methods: Pregnant Sprague-Dawley rats were randomly assigned to no maternal hypoxia or maternal hypoxia treatment groups. Adult male rat offspring were subjected to middle cerebral artery occlusion (MCAO). There were four groups: maternal + sham (MH + Sham), sham (Sham), maternal hypoxia + MCAO (MH + MCAO), and MCAO only (MCAO). Neurological deficits were evaluated. Hippocampal cell damage was observed by hematoxylin and eosin (HE) staining. Cell apoptosis in the hippocampus was detected by TdT-mediated dUTP-biotin nick-end labeling (TUNEL) staining. Caspase-3, cytochrome c, Bax, and bcl-2 expression in the hippocampus was detected by Western blot. Results: More severe hippocampal cell damage was found in the MH + MCAO group than in the MCAO group. Additionally, neurological deficits, percentage of TUNEL positive cells, and expression of caspase-3, cytochrome c, and Bax in the hippocampus were significantly higher (p < 0.05), whereas bcl-2 expression was significantly lower (p < 0.05) in the MH + MCAO group compared to the MCAO group. Conclusions: These findings suggest that maternal hypoxia may exacerbate hippocampal cell apoptosis in rat offspring after MCAO via alterations in the expression of cytochrome c, caspase-3, Bax, and bcl-2, which ultimately affects ischemic stroke prognosis. To our knowledge, this is the first study demonstrating that maternal hypoxia increases hippocampal cell susceptibility to ischemia in adult rat offspring. .

[The effects of prenatal stress on the astrocytes after cerebral ischemia/reperfusion injury in adult offspring rats].

OBJECTIVE: To investigate the effects of prenatal stress on astrocytes after ischemia/reperfusion of cerebral middle artery in adult offspring rats. METHODS: Pregnant rats were randomly assigned to prenatal stress treatment group, which was exposed to restraint three times daily in the last week of pregnancy, and no prenatal stress treatment group. Adult male offspring rats were subjected to transient focal cerebral ischemia by middle cerebral artery occlusion (MCAO). There were three groups:prenatal stress+sham group, MCAO group and prenatal stress+MCAO group (n=10). After 5 days of reperfusion, the infarct size was evaluated. The morphology of astrocytes, co-local-ization of erythropoietin-producing hepatocellular receptor A4 (EphA4) and glial fibrillary acidic protein (GFAP) were detected by double im-munofluorescent staining. And the protein expressions of EphA4, GFAP and Neurocan in peri-ischemic regions were detected by Western blot. RESULTS: The infarct size and the expression of EphA4, GFAP and Neurocan were significantly increased in prenatal stress+MCAO group compared with MCAO group (all P<0.05). And the morphological changes of GFAP-positive astrocytes and co-localization of EphA4/GFAP were more obvious in prenatal stress+MCAO group compared with MCAO group. CONCLUSIONS: Prenatal stress may upregulate the expression of EphA4 on astrocytes in the offspring rats after cerebral ischemia/reperfusion, which promotes the reactivity of astrocyte and increases the ex-pression of neurocan.

Relationships between Prostatic Volume and Intravesical Prostatic Protrusion on Transabdominal Ultrasound and Benign Prostatic Obstruction in Patients with Lower Urinary Tract Symptoms.

INTRODUCTION: The objective of this study is to determine the relationships between prostatic volume (PV) and intravesical prostatic protrusion (IPP) with benign prostatic obstruction (BPO). MATERIALS AND METHODS: A total of 408 males (aged 50 years and above) who presented with lower urinary tract symptoms (LUTS) suggestive of benign prostatic hyperplasia (BPH) were recruited. All had International Prostate Symptoms Score (IPSS), quality of life (QOL) index, uroflowmetry (Qmax) and postvoid residual urine (PVR) measured by transabdominal ultrasonography (TAUS). The PV and the degree of IPP were also measured by TAUS in the transverse and sagittal planes respectively. The PV is classified as Grade a, (20 ml or less), Grade b, (more than 20 ml to 40 ml) and Grade c, (more than 40 ml), while the IPP is graded as Grade 1 (5 mm or less), Grade 2 (more than 5 mm to 10 mm) and Grade 3 (more than 10 mm). RESULTS: There was a fair positive correlation between the PV and IPP (Spearman, r(s) = 0.62, P <0.001) with important clinical exceptions. There was negative correlation between the PV and Qmax (rs = -0.20, P = 0.022), IPP and Qmax (r(s) = -0.30, P <0.001). PV and IPP were good predictors of BPO. However, IPP was slightly better (r(s) of -0.30 vs -0.20) than PV. CONCLUSION: PV is related to IPP with important clinical exceptions. IPP is a better predictor of BPO than PV.

[The effects of prenatal stress on the cell apoptosis after MCAO in adult offspring rats].

OBJECTIVE: To evaluate the effects of prenatal stress on neurological functions after middle cerebral artery occlusion (MCAO) in adult offspring rats. METHODS: Pregnant rats were randomly assigned to prenatal stress treatment, which was exposed to restraint three times daily in the last week of pregnancy, and no prenatal stress treatment. Adult male offspring rats were subjected to transient focal cerebral ischemia by MCAO. They were randomly divided into four groups: sham group, prenatal stress + sham group, MCAO group and prenatal stress + MCAO group (n = 10). After 24 hours of reperfusion, the neurological deficits were evaluated. The infarct size, cell apoptosis and expression of Caspase 3, cleaved Caspase 3 and Bcl-2 were detected. RESULTS: Compared with MCAO group, the neurological deficits, infarct size and apoptotic cells in prenatal stress + MCAO group were increased significantly (all P < 0.05). The expressions of Caspase 3 and cleaved Caspase 3 were much greater in prenatal stress + MCAO group than those of MCAO group, while the expression of Bcl-2 was significantly decreased in prenatal stress + MCAO group compared with MCAO group (all P < 0.05). CONCLUSION: Prenatal stress might exacerbate neuroloeical deficits in the offspring rats after MCAO by increasing cell apoptosis.