pulmonary hypertension syndrome
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2021 ◽  
Vol 11 (1) ◽  
pp. 67-71
Author(s):  
A. V. Yagoda ◽  
A. V. Rybas ◽  
E. N. Danilova ◽  
Yu. V. Gromova

Clinical case of paraneoplastic vasculitis аssociated a brain tumor was presented. Paraneoplastic vasculitis is a rare type of paraneoplastic syndrome. The frequency of detection of paraneoplastic vasculitis in cancer patients is 0.01-5%. In 70% of cases, the manifestation of vasculitis is observed long before the clinical manifestations of the tumor. Most studies report so-called leukocytoclastic vasculitis (allergic) or allergic angiitis. Vasculitis is usually accompanied by slowly progressing tumors such as breast and prostate cancer. It also develops with of stomach cancer, lung cancer, kidney adenocarcinoma, epithelioma, sarcoma, cholangiocarcinoma, other solid tumors, multiple myeloma, non-Hodgkin’s lymphoma. The nosological forms of paraneoplastic vasculitis include called polyarteritis nodosa, hemorrhagic vasculitis, Wegener’s granulomatosis, non-specific aortoarteritis, idiopathic pulmonary hypertension syndrome, thrombovasculitis, allergic hemorrhagic vasculitis, cutaneous vasculitis, systemic necrotizing vasculitis with increased ANCA titer. The patient suffered from paraneoplastic vasculitis with the development of amyloidosis of vascular tissues and arterial hypertension. The progression of the vascular process led to damage of the arteries of the brain and heart, the development of ischemic stroke and hemodynamically significant stenosis of the coronary arteries, the development of acute myocardial infarction complicated by acute heart failure, which caused death. The clinical significance of the case lies in the fact that paraneoplastic vasculitis, which was developed due to a brain astrocytoma with the formation of amyloidosis was firstly described.


Author(s):  
I. N. Maslennikova ◽  
E. L. Bokerija ◽  
I. A. Kazantseva ◽  
T. Yu. Ivanets ◽  
D. N. Degtyarev

The article contains the first-ever data on correlation of the level of N-terminal fragment of natriuretic peptide in the serum of fullterm newborns with circulatory failure and persistent pulmonary hypertension syndrome; while the N-terminal fragment of natriuretic peptide can serve as a marker of circulatory failure in newborns. The study demonstrates that the dynamics of this peptide allows us to evaluate the effectiveness of the therapy.


2018 ◽  
Author(s):  
Khaloud Al-Zahrani ◽  
Timothy Licknack ◽  
Destiny L. Watson ◽  
Nicholas B. Anthony ◽  
Douglas D. Rhoads

AbstractWe have extended our previous survey of the association of mitochondrial prevalence in particular tissues with ascites susceptibility in broilers. We previously reported that in breast muscle of 22 week old susceptible line male birds had significantly higher mtDNA copy number relative to nuclear copy number (mtDNA/nucDNA), compared to resistant line male birds. The higher copy number correlated with higher expression of PPARGC1A mRNA gene. Ascites is a significant metabolic disease associated with fast-growing meat-type chickens (broilers) and is a terminal result of pulmonary hypertension syndrome. We now report the mtDNA/nucDNA ratio in lung, liver, heart, thigh, and breast of both genders at 3, and 20 weeks old. At 3 weeks the mtDNA/nucDNA ratio is significantly higher in lung, breast, and thigh for susceptible line males compared to the resistant line males. Conversely, we see the opposite for lung and breast in females. At 20 weeks of age the differences between males from the two lines is lost for lung, and thigh. Although there is a significant reduction in the mtDNA/nucDNA ratio of breast from 3 weeks to 20 weeks in the susceptible line males, the susceptible males remain higher than resistant line males for this specific tissue. We assessed relative expression of five genes known to regulate mitochondrial biogenesis for lung, thigh and breast muscle from males and females of both lines with no consistent pattern to explain the marked gender and line differences for these tissues. Our results indicate clear sex differences in mitochondrial biogenesis establishing a strong association between the mtDNA quantity in a tissue-specific manner and correlated with ascites-phenotype. We propose that mtDNA/nucDNA levels could serve as a potential predictive marker in breeding programs to reduce ascites.


2018 ◽  
Vol 66 (1) ◽  
pp. 116-124 ◽  
Author(s):  
Behnam Ahmadipour ◽  
Mohammadreza Sharifi ◽  
Fariborz Khajali

This study assessed the preventive effects of arginine (ARG) and guanidinoacetic acid (GAA) on the incidence of pulmonary hypertension syndrome (PHS) in broiler chickens. Four isoenergetic and isonitrogenous diets were prepared, including: (i) the control, (ii) the control supplemented with 1 g/kg ARG, (iii) the control supplemented with 1 g/kg GAA, and (iv) the control supplemented with 1.5 g/kg GAA. These diets were fed to broilers (Ross 308) from day 1 to 42 post-hatch. Criteria evaluated in the experiment were growth performance, carcass characteristics, serum and blood variables, lead-II electrocardiogram, and ET-1 and iNOS gene expression in heart and lungs. Mortality from PHS was recorded daily. The results showed that ARG and GAA supplements improved the feed conversion ratio (FCR) compared to the control (P < 0.05). Supplementation of ARG and GAA significantly (P < 0.05) increased serum nitric oxide (NO) concentration. ARG and GAA supplementation significantly reduced the haematocrit value and the heterophil to lymphocyte ratio in the blood. A significant (P < 0.05) decline in S-wave amplitude of the lead-II electrocardiogram, right to total ventricular weight ratio (RV:TV) and ascites mortality was observed by supplementing ARG or 1.5 g/kg GAA. Addition of ARG and GAA supplements did not significantly change ET-1 and iNOS gene expression in the heart and lung relative to the control. In conclusion, GAA supplementation at 1.5 g/kg had a potential to improve growth performance and could prevent PHS.


2016 ◽  
Vol 94 (4) ◽  
pp. 1493-1500 ◽  
Author(s):  
M. Kamely ◽  
M. A. Karimi Torshizi ◽  
S. Rahimi ◽  
R. F. Wideman

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