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1.
Eur Rev Med Pharmacol Sci ; 22(19): 6448-6455, 2018 10.
Article in English | MEDLINE | ID: mdl-30338813

ABSTRACT

OBJECTIVE: To investigate the changes as well as the related mechanism in cognitive function and levels of serum ß-amyloid peptide (Aß) and brain-derived neurotrophic factor (BDNF) in stroke patients. PATIENTS AND METHODS: A total of 30 patients with acute stroke treated in our hospital from June 2015 to September 2016 were selected as stroke group, while 30 volunteers during the same period were enrolled as control group. Changes in cognitive function of patients were evaluated using the Montreal Cognitive Assessment (MoCA) and mini-mental state examination (MMSE) before and after the treatment. At the same time, the concentrations of serum Aß1-40 and BDNF were detected, and their correlations with the MMSE score were analyzed. Finally, levels of serum cyclic adenosine monophosphate (cAMP) and phosphorylated-cAMP-response element binding protein (p-CREB), and the phosphorylation level of Tau protein were detected by Western blotting. RESULTS: MoCA and MMSE scores of patients in stroke group were significantly lower than those in control group (p < 0.01), and the scores were significantly higher in stroke patients after treatment than those before treatment (p < 0.01). Compared with those in control group, the serum Aß1-40 concentration in patients in stroke group was significantly increased (p < 0.01), but the BDNF level was significantly decreased (p < 0.01). Compared with those before treatment, the serum Aß1-40 concentration in patients was significantly decreased after treatment (p < 0.01), but the BDNF concentration was significantly increased (p < 0.01). Correlation analysis showed that the MMSE score was negatively correlated with the concentration of Aß1-40 (r2 = 0.764, p < 0.01), but positively related to the level of BDNF (r2 = 0.827, p < 0.01). Compared with those in control group, the content of serum cAMP and p-CREB in stroke patients was significantly decreased (p < 0.01), but the expression of p-Tau was statistically increased (p < 0.01). CONCLUSIONS: The cognitive function in stroke patients is impaired, with the rising content of serum Aß1-40 and reduction of BDNF, the mechanism of which is related to the decrease of cAMP and p-CREB and the increase of p-Tau. This provides a theoretical basis for searching the new therapeutic targets and new drugs for stroke.


Subject(s)
Amyloid beta-Peptides/blood , Brain-Derived Neurotrophic Factor/blood , Cognition , Peptide Fragments/blood , Stroke/blood , Aged , Biomarkers/blood , Case-Control Studies , Cyclic AMP/blood , Cyclic AMP Response Element-Binding Protein/blood , Female , Humans , Male , Middle Aged , Phosphorylation , Prognosis , Stroke/diagnosis , Stroke/psychology , Stroke/therapy , Time Factors , tau Proteins/blood
2.
West Indian Med J ; 65(1): 232-235, 2015 Jun 09.
Article in English | MEDLINE | ID: mdl-26633137

ABSTRACT

AIM: To use computed tomography (CT) to diagnose the reasons for hepatic portal venous gas (HPVG) in the case of an elderly male patient. METHODS: This is a case study of an elderly male patient who suffered acute, obvious abdominal pain accompanied with stop of exhaust defecation following three days of diarrhoea, abdominal distention and emesis. The patient also developed asthma, which gradually became severe. The patient was admitted to the hospital where he underwent a physical examination and a CT scan. RESULTS: The CT results confirmed that the patient was suffering from HPVG caused by severe diarrhoea. The CT scan showed obvious expansion and pneumatosis in the enteric cavity and subcutaneous emphysema in the intestinal wall. Also, the intrahepatic portal branches and small branches of veins in the mesentery were filled with a high density of gas. The combination of many factors led to HPVG. Gastrointestinal mucosa and pressure accompanied with intestinal septic infection were the main factors. The case report revealed that gas in the enteric cavity went into the submucosa, then into the small branches of veins in the mesentery and finally into the intrahepatic portal vein system. CONCLUSIONS: Computed examination revealed the imaging features of HPVG. Hepatic portal venous gas suggested the growth of enteric cavity pressure, the damage of intestinal mucosa and intestinal infection, providing references for clinical diagnosis.

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