Clinical features and misdiagnosis analysis of children with cerebral paragonimiasis with intracranial hemorrhage as initial symptom / 中华实用儿科临床杂志

Objective To explore the clinical characteristics and the cause of misdiagnosis of child suffering from cerebral parago-nimiasis with intracranial hemorrhage as initial symptom,and to improve the diagnosis and treatment level of cerebral paragonimiasis.Methods The clinical data of the children who suffered from cerebral paragonimiasis with intracranial hemorrhage as initial symptom were collected from January 2011 to December 2015 in Affiliated Hospital of Zunyi Medical College.The clinical manifestation,imageology and laboratory tests,outcome of therapy were analyzed and then the effect of treatment and the prognosis were followed up.Results There were 7 patients meeting the inclusion criteria for cerebral paragonimiasis,including 4 male and 3 female.They were from 6 to 13 years old with the average age of 9.3 years old.All patients presented with headache and vomiting,and showed intracranial hemorrhage through CT or MRI of brain.All of the 7 patients were misdiagnosed as cerebrovascular malformation by the neurosurgeons.Three of them showed typical imaging pattern including tunnel sign and the ring-like shape of cerebral paragonimiasis.Five of these cases were attacked by pulmonary distomiasis at the same time.Six of them had an increasing eosinophil,and the paragonimus antibody was positive.They were treated with Praziquantel.Six patients recovered completely,and 1 patient had the dysfunction of left extremities.Conclusions The childhood cerebral paragonimiasis has strong clinical heterogeneity and diversity in manifestation.Intracranial hemorrhage may be the initial symptom,which should be paid more attention to.Cerebral paragonimiasis can be diagnosed and treated early according to the clinical characteristics,the increase of eosinophil,the typical changes in imageology and the specific antibody test.

Effects of different angiotensin II type 1 receptor blockers on regulation of ACE-Ang II-AT1 and ACE2-Ang(1-7)-Mas axes in pressure overload-induced cardiac remodeling in male mice / 中国病理生理杂志

AIM:To examine and compare the effects of several ARBs that are widely used in clinics , on the ACE-Ang II-AT1 receptor and the ACE2-Ang(1-7)-Mas axis during the development of cardiac remodeling after pressure overload .METHODS: All of the mice used in the study underwent transverse aortic constriction (TAC) or sham operation for 2 or 4 weeks.A solution of either ARBs or sa-line was administered through a stomach tube 3 days before the operation .Meanwhile , to eliminate the influence of Ang II , a recombi-nant adenovirus expressing small interfering RNAs targeting angiotensinogen ( Ad-ATG siRNA) was injected via the tail vein .The sur-gery was then performed and the drug was administered as mentioned above .Cardiac function and remodeling were evaluated by echo-cardiography , hemodynamic measurements and cardiac histology .Western blotting was used to determine the protein expression levels . Meanwhile , we performed similar experiments using ARBs with or without ATG siRNA in cardiomyocytes induced by mechanical stretch.RESULTS:Although all of the six ARBs , none of which repressed the elevation of left ventricular pressure after TAC , attenu-ated the development of cardiac hypertrophy and heart failure in the wild-type mice, the degree of attenuation by Olmesartan , Candesar-tan and Losartan tended to be larger than that of the other three drugs tested .Additionally , the degree of downregulation of the ACE-Ang II-AT1 axis and upregulation of the ACE2-Ang(1-7)-Mas axis was higher in response to Olmesartan, Candesartan and Losartan administration in vivo and in vitro.Additionally, Olmesartan had a larger influence when administered long term .However, the expres-sion of ACE was not influenced by the administration of ARBs in vivo and in vitro.Moreover, in angiotensinogen-knockdown mice, TAC-induced cardiac hypertrophy and heart failure were inhibited by Olmesartan , Candesartan and Losartan but not by Telmisartan , Valsartan and Irbesartan administration .Furthermore , only Olmesartan and Candesartan could downregulate the ACE-Ang II-AT1 axis and upregulate the ACE2-Ang(1-7)-Mas axis in vitro.CONCLUSION: Olmesartan, Candesartan and Losartan could effectively in-hibit pressure overload-induced cardiac remodeling even when with knockdown of Ang II , possibly through upregulation of the expres-sion of the ACE2-Ang(1-7)-Mas axis and downregulation of the expression of the ACE-Ang II-AT1 axis.In contrast, Telmisartan, Valsartan and Irbesartan only played a role in the presence of Ang II , and Losartan had no effect in the presence of Ang II in vitro.

Angiotensin II type 1 receptor is required for the cardiac fibrosis triggered by mechanical stress independent of Ang II in mice / 中国病理生理杂志

AIM:We investigated how AT 1-R stimulated by mechanical stresses induces cardiac fibrosis .METHODS:We produced in vivo cardiac pressure overload model in angiotensinogen knockout ( ATG-/-) mice and in vitro mechanically-stretched cell model in cultured neonatal cardiac cells of ATG-/-mice both lack the participation of Ang II .RESULTS: Pressure overload for 4 weeks in ATG-/-mice induced myocardial hypertrophy accompanied by the significant interstitial fibrosis , however , the TGF-β, a key regulatory factor of fibrosis, was not significantly increased in these ATG-/-mice.Meanwhile, the inhibitor for AT1-R significantly inhibited mechani-cal stress-induced cardiac fibrosis in these ATG-/-models whereas inhibition of TGF-βdid not.CONCLUSION:The results showed that mechanical stress-induced fibrotic responses through AT 1-R required the phosphorylation of Smad 2 but not the involvement of TGF-β.