• Annals of Clinical Neurophysiology
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• v.25 no.1
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• pp.32-37
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• 2023

Background: Type 2 diabetic mellitus (T2DM) is an emerging global pandemic which is associated with lots of co-morbidities and reported vascular dysfunctions. T2DM associated vascular dysfunctions leads to vasculopathy in the form of altered peripheral vascular dynamics. Cold stress test (CST) is a reliable sympathetic reactivity test used for assessing vascular dysfunctions. In this study we are trying to quantify vascular dysfunctions in T2DM patients non invasively by various parameters of photoplethysmography (PPG) of cold stress test. Methods: Case control study had done in referral health center AIIMS, Raipur. Parameters are recorded by finger-PPG before, during and after CST (1 min) in 2 groups, control (n = 20 healthy volunteers) and case (n = 20 diagnosed T2DM patients). Results: Due to cold stress, PPG parameter peak amplitude was significantly decreased in both healthy and T2DM groups (p <0.001 and p <0.001, respectively). However, recovery trend of amplitude was significantly slow in T2DM compared to healthy subjects. Another PPG parameter peak to peak interval was significantly higher in healthy group compared to T2DM patients. Conclusions: This study showed that T2DM patients has significant deranged pulse volume parameters like amplitude and peak to peak interval can be used to objectively quantify the vasculopathy in T2DM patients by using sympathetic reactivity to cold stress.

• Journal of Yeungnam Medical Science
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• v.40 no.3
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• pp.225-232
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• 2023

Cognitive dysfunction is relatively less considered a complication of hypertension. However, there is sufficient evidence to show that high blood pressure in middle age increases the risk of cognitive decline and dementia in old age. The greatest impact on cognitive function in those with hypertension is on executive or frontal lobe function, similar to the area most damaged in vascular dementia. Possible cognitive disorders associated with hypertension are vascular dementia, Alzheimer disease, and Lewy body dementia, listed in decreasing strength of association. The pathophysiology of cognitive dysfunction in individuals with hypertension includes brain atrophy, microinfarcts, microbleeds, neuronal loss, white matter lesions, network disruption, neurovascular unit damage, reduced cerebral blood flow, blood-brain barrier damage, enlarged perivascular damage, and proteinopathy. Antihypertensive drugs may reduce the risk of cognitive decline and dementia. Given the high prevalence of dementia and its impact on quality of life, treatment of hypertension to reduce cognitive decline may be a clinically relevant intervention.

• Clinical and Experimental Pediatrics
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• v.57 no.11
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• pp.472-478
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• 2014

Kawasaki disease (KD), an acute vasculitis that primarily affects young children, is the most common acquired paediatric cardiovascular disease in developed countries. While sequelae of arterial inflammation in the acute phase of KD are well documented, its late effects on vascular health are increasingly unveiled. Late vascular dysfunction is characterized by structural alterations and functional impairment in term of arterial stiffening and endothelial dysfunction and shown to involve both coronary and systemic arteries. Further evidence suggests that continuous low grade inflammation and ongoing active remodeling of coronary arterial lesions occur late after acute illness and may play a role in structural and functional alterations of the arteries. Potential importance of genetic modulation on vascular health late after KD is implicated by associations between mannose binding lectin and inflammatory gene polymorphisms with severity of peripheral arterial stiffening and carotid intima-media thickening. The changes in cholesterol and lipoproteins levels late after KD further appear similar to those proposed to be atherogenic. While data on adverse vascular health are less controversial in patients with persistent or regressed coronary arterial aneurysms, data appear conflicting in individuals with no coronary arterial involvements or only transient coronary ectasia. Notwithstanding, concerns have been raised with regard to predisposition of KD in childhood to accelerated atherosclerosis in adulthood. Until further evidence-based data are available, however, it remains important to assess and monitor cardiovascular risk factors and to promote cardiovascular health in children with a history of KD in the long term.

• Korean Journal of Biological Psychiatry
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• v.23 no.3
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• pp.80-88
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• 2016

Vascular dementia is a very frequent form of dementia. Debates over classification and diagnostic criteria, and controversy over identifiable treatment targets will continue until distinct pathophysiological mechanism of vascular dementia is found. Clinical diagnostic criteria are sufficiently strong to be useful for clinical trials, but need further refinement. Cognitive changes in vascular dementia are more variable than other disorders, and are dependent on the vascular pathology. Accurate diagnosis of vascular dementia is known to need the presence of reliable cerebrovascular disease on brain imaging. Although it seems obvious that cerebrovascular disease causes pathological damage and impaired cognition, it is very difficult to find the accurate contribution of cerebrovascular pathology to cognitive decline. Most studies have shown a small but significant benefit of cholinesterase inhibitors on cognition, the significance of this effect has been slight and benefits on global functioning, activities of daily living, and behaviour have not been consistently reported. Management of vascular dementia should focus on identifying and managing vascular risk factors.

• Journal of Yeungnam Medical Science
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• v.36 no.3
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• pp.183-191
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• 2019

Some patients with type 1 and type 2 diabetes mellitus (DM) present with cognitive dysfunctions. The pathophysiology underlying this complication is not well understood. Type 1 DM has been associated with a decrease in the speed of information processing, psychomotor efficiency, attention, mental flexibility, and visual perception. Longitudinal epidemiological studies of type 1 DM have indicated that chronic hyperglycemia and microvascular disease, rather than repeated severe hypoglycemia, are associated with the pathogenesis of DM-related cognitive dysfunction. However, severe hypoglycemic episodes may contribute to cognitive dysfunction in high-risk patients with DM. Type 2 DM has been associated with memory deficits, decreased psychomotor speed, and reduced frontal lobe/executive function. In type 2 DM, chronic hyperglycemia, long duration of DM, presence of vascular risk factors (e.g., hypertension and obesity), and microvascular and macrovascular complications are associated with the increased risk of developing cognitive dysfunction. The pathophysiology of cognitive dysfunction in individuals with DM include the following: (1) role of hyperglycemia, (2) role of vascular disease, (3) role of hypoglycemia, and (4) role of insulin resistance and amyloid. Recently, some investigators have proposed that type 3 DM is correlated to sporadic Alzheimer's disease. The molecular and biochemical consequences of insulin and insulin-like growth factor resistance in the brain compromise neuronal survival, energy production, gene expression, plasticity, and white matter integrity. If patients claim that their performance is worsening or if they ask about the effects of DM on functioning, screening and assessment are recommended.

• Biomolecules & Therapeutics
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• v.24 no.5
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• pp.523-528
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• 2016

Urotensin II (UII) is a potent vasoactive peptide and mitogenic agent to induce proliferation of various cells including vascular smooth muscle cells (VSMCs). In this study, we examined the effects of a novel UII receptor (UT) antagonist, KR-36676, on vasoconstriction of aorta and proliferation of aortic SMCs. In rat aorta, UII-induced vasoconstriction was significantly inhibited by KR-36676 in a concentration-dependent manner. In primary human aortic SMCs (hAoSMCs), UII-induced cell proliferation was significantly inhibited by KR-36676 in a concentration-dependent manner. In addition, KR-36676 decreased UII-induced phosphorylation of ERK, and UII-induced cell proliferation was also significantly inhibited by a known ERK inhibitor U0126. In mouse carotid ligation model, intimal thickening of carotid artery was dramatically suppressed by oral treatment with KR-36676 (30 mg/kg/day) for 4 weeks compared to vehicle-treated group. From these results, it is indicated that KR-36676 suppress UII-induced proliferation of VSMCs at least partially through inhibition of ERK activation, and that it also attenuates UII-induced vasoconstriction and vascular neointima formation. Our study suggest that KR-36676 may be an attractive candidate for the pharmacological management of vascular dysfunction.

• BMB Reports
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• v.52 no.2
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• pp.145-150
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• 2019

Endothelial dysfunction-induced lipid retention is an early feature of atherosclerotic lesion formation. Apoptosis of vascular smooth muscle cells (VSMCs) is one of the major modulating factors of atherogenesis, which accelerates atherosclerosis progression by causing plaque destabilization and rupture. However, the mechanism underlying VSMC apoptosis mediated by endothelial dysfunction in relation to atherosclerosis remains elusive. In this study, we reveal differential expression of several genes related to lipid retention and apoptosis, in conjunction with atherosclerosis, by utilizing a genetic mouse model of endothelial nitric oxide synthase (eNOS) deficiency manifesting endothelial dysfunction. Moreover, eNOS deficiency led to the enhanced susceptibility against pro-apoptotic insult in VSMCs. In particular, the expression of aggrecan, a major proteoglycan, was elevated in aortic tissue of eNOS deficient mice compared to wild type mice, and administration of aggrecan induced apoptosis in VSMCs. This suggests that eNOS deficiency may elevate aggrecan expression, which promotes apoptosis in VSMC, thereby contributing to atherosclerosis progression. These results may facilitate the development of novel approaches for improving the diagnosis or treatment of atherosclerosis.

• Clinical and Experimental Pediatrics
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• v.56 no.3
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• pp.130-134
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• 2013

Purpose: Anthracyclines have been utilized in the treatment of children with acute lymphoblastic leukemia (ALL). Recent studies have shown that anthracyclines may induce toxicity in the vascular endothelium. This study was performed using brachial artery reactivity (BAR) to evaluate vascular endothelial function in ALL patients who were treated with anthracycline chemotherapy. Methods: We included 21 children with ALL who received anthracycline chemotherapy and 20 healthy children. The cumulative dose of anthracyclines in the ALL patients was $142.5{\pm}18.2/m^2$. The last anthracycline dose was administered to the patients 2 to 85 months prior to their examination using BAR. The diameter of the brachial artery was measured in both groups using echocardiography, and BAR was calculated as the percentage change in the arterial diameter after release of the cuff relative to the baseline vessel diameter. Results: In the anthracycline-treated group, BAR was observed to be $3.4%{\pm}3.9%$, which was significantly lower than that observed in the control group ($12.1%{\pm}8.0%$, P<0.05). The time elapsed after the last anthracycline treatment and the age at the time of treatment did not affect the change in BAR (P =0.06 and P =0.13, respectively). Conclusion: These results provided evidence that treatment of ALL patients with anthracycline results in endothelial dysfunction. A larger cohort study and a longer follow-up period will be required to clarify the relationship between endothelial dysfunction resulting from anthracycline treatment for childhood ALL and occurrence of cardiovascular diseases later in life.

• Journal of Korean Neurosurgical Society
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• v.47 no.4
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• pp.282-286
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• 2010

Objective : The aim of the present study was to assess the effect of lumbar disc herniation surgery for low back pain on the erectile functioning. Methods : Thirty-eight patients, with age ranging from 22 to 56 years, who had presented with pain due to herniated lumbar discs were included in the study. International Index of Erectile Function (IIEF) Short Form questionnaire was used to evaluate the erectile functioning. Patient visits on the 1st week,1st month and 3rd month postoperatively were analyzed. Pain scores were also noted together with side effects and the complications of the surgery. Results : Of the 38 patients, 18 patients had reported erectile dysfunction; 10 patients mild and 8 patients moderate erectile dysfunction. Twenty patients did not report erectile problems. The herniation levels mostly were L5-S1 in 12 (31.6%). Overall, erectile dysfunction rates have improved in 31.7% of those previously with erectile dysfunction in a 3 month period after the surgery. Best results were obtained in those patients with mild erectile dysfunction preoperatively. Conclusion : Mild erectile dysfunction together with radiculopathy tends to improve after lumbosacral disc surgery. Moderate and severe erectile dysfunction may be related to a more severe nerve injury or to vascular and/or psychiatric factors. An evaluation of erectile functioning should routinely be performed in patients with lumbosacral disc disease both for data accumulation and for medico legal causes since the documentation of the correlation between erectile dysfunction and lumbosacral disc disease is still lacking.

• BMB Reports
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• v.47 no.1
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• pp.1-7
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• 2014

Atherosclerosis is a pathologic process occurring within the artery, in which many cell types, including T cell, macrophages, endothelial cells, and smooth muscle cells, interact, and cause chronic inflammation, in response to various inner- or outer-cellular stimuli. Atherosclerosis is characterized by a complex interaction of inflammation, lipid deposition, vascular smooth muscle cell proliferation, endothelial dysfunction, and extracellular matrix remodeling, which will result in the formation of an intimal plaque. Although the regulation and function of vascular smooth muscle cells are important in the progression of atherosclerosis, the roles of smooth muscle cells in regulating vascular inflammation are rarely focused upon, compared to those of endothelial cells or inflammatory cells. Therefore, in this review, we will discuss here how smooth muscle cells contribute or regulate the inflammatory reaction in the progression of atherosclerosis, especially in the context of the activation of various membrane receptors, and how they may regulate vascular inflammation.