Sexual dimorphism in arterial hypertension: an age-related phenomenon

2000 ◽  
Vol 29 (3) ◽  
pp. 283-289 ◽  
Author(s):  
Roberto Antonicelli ◽  
Rosaria Gesuita ◽  
Enrico Paciaroni
2021 ◽  
Vol 22 (15) ◽  
pp. 8111
Author(s):  
Kuang-Hsu Lien ◽  
Chao-Hui Yang

The triad of noise-generated, drug-induced, and age-related hearing loss is the major cause of acquired sensorineural hearing loss (ASNHL) in modern society. Although these three forms of hearing loss display similar underlying mechanisms, detailed studies have revealed the presence of sex differences in the auditory system both in human and animal models of ASNHL. However, the sexual dimorphism of hearing varies among noise-induced hearing loss (NIHL), ototoxicity, and age-related hearing loss (ARHL). Importantly, estrogen may play an essential role in modulating the pathophysiological mechanisms in the cochlea and several reports have shown that the effects of hormone replacement therapy on hearing loss are complex. This review will summarize the clinical features of sex differences in ASNHL, compare the animal investigations of cochlear sexual dimorphism in response to the three insults, and address how estrogen affects the auditory organ at molecular levels.


2008 ◽  
Vol 132 (8) ◽  
pp. 1329-1332
Author(s):  
Anna K. Wong ◽  
Belle Fang ◽  
Ling Zhang ◽  
Xiuqing Guo ◽  
Stephen Lee ◽  
...  

Abstract Context.—The clinical association between loss of the Y chromosome and acute myelogenous leukemia and myelodysplastic syndrome (AML/MDS) has been debated because both phenomena are related to aging. A prior publication suggests that loss of the Y chromosome in more than 75% of cells may indicate a clonal phenomenon that could be a marker for hematologic disease. Objective.—To evaluate the relationship between loss of the Y chromosome and AML/MDS. Design.—A retrospective review of cytogenetic reports of 2896 male patients ascertained from 1996 to 2007 was performed. Results were stratified based on the percentage of cells missing the Y chromosome and were correlated with patients' ages and bone marrow biopsy reports through logistic regression analysis with adjustment for age. Results.—Loss of the Y chromosome was found in 142 patients. Of these, 16 patients demonstrated myeloid disease, with 2 cases of AML and 14 cases of MDS. An increased incidence (P < .05) of AML/MDS was seen only in the group composed of 8 patients with complete loss of the Y chromosome in all karyotyped cells (1 case of AML and 7 cases of MDS). Conclusion.—Loss of the Y chromosome appears to be primarily an age-related phenomenon. However, in individuals in which all cells on cytogenetic analysis showed loss of the Y chromosome, there was a statistically significant increase in AML/MDS, suggesting that the absence of any normal-dividing cells in a bone marrow analysis may be indicative of AML/MDS.


2019 ◽  
Vol 23 (2) ◽  
pp. 277-282
Author(s):  
V. D. Nemtsova ◽  
I. A. Ilchenko ◽  
V. V. Zlatkina

Due to the growing number of patients with age-related diseases, the aim of the study was to investigate in the changes of aging rate (AR) in patients with comorbid course of arterial hypertension (H), type 2 diabetes mellitus (T2DM) and subclinical hypothyroidism (SH) and to study the features of these changes depending on hormonal imbalance. 118 patients (63 women and 55 men, average age — 53.6±4.3 years) were divided into 3 groups: group 1 (n=37) with isolated H; group 2 (n=42) — with H and T2DM; group 3 (n=39) — with H, T2DM and SH. The investigation program included: measurement of anthropometric parameters (blood pressure, height, body weight (BW), body mass index (BMI)), carbohydrate and thyroid metabolism using standard methods, biological age (BA) by V.P. Voitenko et al. Statistical processing was performed using the Statistica for Windows 8.0 software package. When evaluating AR, physiological aging was found in 8 patients (21.6%) of group 1, in 4 (9.5%) patients of group 2 and 3 (7.7%) of patients in group 3. In the overwhelming majority of the examined patients, premature aging (PA) was noted, however, the acceleration of PA between patients of groups 2 and 3 was not differ significantly (p>0.05). The increase in AR in group 2 patients was accompanied by an increase in BA by 7.2 years, in 3 group patients — by 7.3 years compared with their chronological age. A correlation analysis revealed a positive relationship between BMI and coefficient of aging rate (CAR) (r=0.679; p<0.05); BMI and BA (r=0.562; p<0.05) and CAR and the TSH level (r=0.050; p=0.388) in the 3rd group. Thus, the presence of hypertension and comorbid endocrinopathies — T2DM and SH significantly increases the AR and when assessing the effect of endocrine disorders, the presence of T2DM is more important than SH.


Author(s):  
Denisha R Spires ◽  
Oleg Palygin ◽  
Vladislav Levchenko ◽  
Elena Isaeva ◽  
Christine A. Klemens ◽  
...  

Diabetic kidney disease (DKD) is a common complication of diabetes, which frequently leads to end-stage renal failure and increases cardiovascular disease risk. Hyperglycemia promotes renal pathologies such as glomerulosclerosis, tubular hypertrophy, microalbuminuria, and a decline in glomerular filtration rate. Importantly, recent clinical data have demonstrated distinct sexual dimorphism in the pathogenesis of DKD in people with diabetes, which impacts both severity- and age-related risk factors. This study aimed to define sexual dimorphism and renal function in a non-obese type 2 diabetes model with the spontaneous development of advanced diabetic nephropathy (T2DN rats). T2DN rats at 12- and over 48-weeks old were used to define disease progression and kidney injury development. We found impaired glucose tolerance and glomerular hyperfiltration in T2DN rats to compare with non-diabetic Wistar control. The T2DN rat displays a significant sexual dimorphism in insulin resistance, plasma cholesterol, renal and glomerular injury, urinary nephrin shedding, and albumin handling. Our results indicate that both male and female T2DN rats developed non-obese type 2 DKD phenotype, where the females had significant protection from the development of severe forms of DKD. Our findings provide further evidence for the T2DN rat strain's effectiveness for studying the multiple facets of DKD.


2015 ◽  
Vol 53 (2) ◽  
pp. 184-192 ◽  
Author(s):  
Akina Nara ◽  
Hisashi Nagai ◽  
Kaori Shintani-Ishida ◽  
Sayoko Ogura ◽  
Tatsuo Shimosawa ◽  
...  

Author(s):  
Özlem Gögebakan ◽  
Martin Osterhoff ◽  
Thomas Albrecht

Background Mesenteric panniculitis (MP) is histologically characterized by chronic nonspecific inflammation of the adipose tissue of the intestinal mesentery with unclear etiology. MP occurs predominantly in men, mostly in mid to late adulthood. MP is typically found as an incidental diagnosis on abdominal CT. Methods A comprehensive review of the literature including case reports and cohort studies was performed. Therefore, a global search in PubMed was carried out. Search terms were (and/or) “mesenteric panniculitis”, “panniculitis mesenterialis”, “mesenteric lymph nodes”, “CT”, “imaging”, “sclerosing mesenteritis”, “case report”, “therapy”. Results and Conclusion MP is a relatively common CT finding. The true prevalence seems to be higher than the reported 0.6 % to 2.4 % due to underreporting. The most important differential diagnosis is malignant lymphoma, which may be difficult to distinguish from MP. The majority of patients with MP are clinically asymptomatic and do not require therapy. In rare symptomatic cases, non-specific symptoms like abdominal pain, fever, nausea or vomiting occur. For therapy, glucocorticoids and tamoxifen have been suggested. Several studies suggested that MP is associated with other diseases and might be a paraneoplastic phenomenon, but four recently published case-control studies suggest that MP is an independent non-specific benign age-related phenomenon. However, two further studies show a possible association of MP with malignant lymphoma. The clinical relevance of MP remains the subject of scientific debate. Key Points:  Citation Format


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Aimo ◽  
A Gimelli ◽  
G Vergaro ◽  
D Genovesi ◽  
A Kusch ◽  
...  

Abstract Background Tissue accumulation of misfolded transthyretin (TTR) may occur because of TTR gene mutations (variant amyloid TTR amyloidosis, ATTRv), or as an age-related phenomenon (wild-type ATTR, ATTRwt). Cardiac sympathetic denervation has been reported in ATTRv, but has never been investigated in ATTRwt. Methods Fifteen consecutive patients with ATTRwt cardiomyopathy (81% men, median age 82 years, no one with prior myocardial infarction) underwent Cadmium Zinc Telluride tomographic imaging for amyloid burden (99mTc-hydroxymethylene diphosphonate - 99mTc-HMDP), innervation (123I-metaiodobenzylguanidine – 123I-MIBG), and perfusion (99mTc-tetrofosmin). Results Median summed 99mTc-HMDP score was 60 (58–62), denoting a severe and diffuse amyloid burden. Planar 123I-MIBG examination showed decreased early and late H/M ratios (late H/M ratio: 1.5 [1.3–1.6], range 1.2–1.9, reference value ≥2.0). Summed 123I-MIBG score was 12 (6–22), with the most prominent denervation in the infero-septal, inferior, and infero-lateral regions; summed rest score was 7 (5–11), with lowest degrees of myocardial perfusion in the inferior and infero-septal regions. The correlation between amyloid burden (as relative 99mTc-HMDP uptake) and innervation (as relative 123I-MIBG uptake) did not achieve statistical significance at both segmental (p=0.252) and regional level (p=0.251). Nevertheless, denervation tended to worsen in parallel with the amyloid burden, and 123I-MIBG scores increased with 99mTc-HMDP scores. Segments and regions with more prominent hypoperfusion were those showing the more intense denervation (r=0.500 and 0.591, respectively; both p&lt;0.001). Conclusions Patients with ATTRwt cardiomyopathy display cardiac sympathetic denervation, particularly in the inferior and septal myocardial wall. Myocardial hypoperfusion has a similar regional pattern, while the amyloid burden is more extensive. Funding Acknowledgement Type of funding source: None


1986 ◽  
Vol 39 (3) ◽  
pp. 123-127 ◽  
Author(s):  
Karsten Thomsen ◽  
Anders Gotfredsen ◽  
Claus Christiansen

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