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- SourceAvailable from: Miroslav Stefanov[Show abstract] [Hide abstract]
ABSTRACT: Traditional Eastern medicine has had a successful existence for a long time and has provided functional paths for curing disease. However, some scientists do not accept acupuncture, primarily because the meridian system lacks a physical anatomical basis. To date, scientific theories have not been able to explain the functional paths used by traditional Eastern medicine to cure disease. According to Western medicine, no known anatomical foundation exists for the meridians and unknown nervous, circulatory, endocrine, and immune mechanisms mediate the effects of acupuncture. In the early 1960s, only one hypothesis was proposed to explain the anatomical basis of the meridians. By using different experimental approaches during the past 10 years, the number of scientific papers that report the discovery of different anatomical and physiological evidence confirming the existence of an anatomical basis for the meridian system has increased. Morphological science is greatly challenged to offer a new biomedical theory that explains the possible existence of new bodily systems such as the primo vascular system (PVS). The PVS is a previously unknown system that integrates the features of the cardiovascular, nervous, immune, and hormonal systems. It also provides a physical substrate for the acupuncture points and meridians. Announcements of the morphological architectonics and the function of the PVS fundamentally changed the basic understanding of biology and medicine because the PVS is involved in the development and the functions of living organisms. We propose a new vision of the anatomical basis for the PVS and the vital energy-called "Qi"-as an electromagnetic wave that is involved very closely with the DNA in the PVS. DNA provides genetic information and it functions as a store of information that can be obtained from the electromagnetic fields of the environment. The PVS is the communication system between living organisms and the environment, and it lies at the lowest level of life. The theory of the PVS could be a good basis for forming a new point of view of Darwin's evolutionary theory. Discoveries in morphological theory-such as discoveries with respect to the PVS-have not been made since the 18th century. For that reason, the PVS needs more attention.12/2013; 6(6):331-8. DOI:10.1016/j.jams.2013.10.001
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ABSTRACT: Clinical significance of autoantibodies to parietal cells (PCA) in patients with autoimmune thyroid diseases (ATD) remains contradictory. To characterize the frequency of PCA in patients with ATD; to clarify the role of gender and age in PCA positivity; to analyze the association of PCA with gastric or haematologic symptoms and with the levothyroxine dose required to achieve a serum TSH level within the normal range in treated Hashimoto's thyroiditis (HT) patients. PCA were measured using ELISA in 137 HT patients, divided into tree subgroups according to the thyroid function: group I included subjects with normal thyroid function; group II included patients with hypothyroidism, in group III were enrolled subjects treated with levothyroxine (LT4). We also studied the PCA positivity in 14 patients with active Graves' disease and in 23 healthy controls. PCA positivity was found in 51 patients with autoimmune thyroid diseases, with an overall prevalence of 33.8%. No significant differences in PCA were observed between the groups of HT patients. The frequency of PCA in both genders was similar and there were no difference depending on age. In 7.3% of HT patients in different stages of disease we found clinically relevant gastric and/or haematologic symptoms; in 70% of them PCA were positive (OR = 5.5; 95% CI: 1.2 - 28.4; p = 0.009). PCA positive hypothyroid HT patients required higher LT4 doses than PCA negative (1.46 microg/kg vs 1.24 microg/kg, p = 0.04). PCA may be present in different stages in HT patients; this does not depend on the severity of disease. PCA concentrations may predict symptoms of atrophic gastritis in patients with Hashimoto's thyroiditis. PCA positive HT patients require higher replacement doses of LT4. Presence of anemia, particularly microcytic anemia, was suggestive of undiagnosed atrophic gastritis.Folia medica 11/2013; 55(2):26-32. DOI:10.2478/folmed-2013-0014
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ABSTRACT: It has been well defined that obesity is strongly linked with several respiratory symptoms and diseases, but no convincing evidence has been provided for chronic obstructive pulmonary disease (COPD). In the current study, we aim to assess the possible prevalence of obesity in patients with COPD in a cross-sectional case-control study of individuals from the region of Stara Zagora, Bulgaria, and to explore whether the body mass has some effect on the lung function of COPD patients. The study included 158 patients with COPD (Global Initiative for Chronic Obstructive Lung Disease (GOLD) II, III, and IV stages) and 123 individuals unaffected by the disease (control). A higher frequency of obesity compared to the controls (20.3%) was observed in patients with COPD (29.1%, p = 0.093), especially in those with GOLD II stage (37.7%, p = 0.009). Prevalence of obesity was highest in COPD GOLD II, followed by GOLD III and IV stages (p = 0.068). When diabetes was considered as confounding factor, we found a significant prevalence of obesity in COPD patients than the controls with diabetes (p = 0.031). Interestingly, there was a statistically significant moderate positive correlation between the body mass index and forced expiratory volume in one second as a percentage of predicted value in the whole patients' group (R = 0.295, p = 0.0002) as well as in the subgroups of GOLD II (R = 0.257, p = 0.024) and GOLD III COPD (R = 0.259, p = 0.031).The results of our study propose that the increased body mass, particularly obesity is frequent comorbidity to COPD, especially to less severe diseases. Moreover, the results suggest that the higher body weight may provide some protection against the impairment of lung functions in patients with stable COPD.Chronic Respiratory Disease 09/2013; 10(4). DOI:10.1177/1479972313504940
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