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Dr. Konstantina  Kritikos-Karalis  Dmd image

Dr. Konstantina Kritikos-Karalis Dmd

117 N Furnace St
Birdsboro PA 19508
610 821-1594
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: DS029973L
NPI: 1235322652
Taxonomy Codes:
1223G0001X

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Clinical features and polysomnographic findings in greek male patients with obstructive sleep apnea syndrome: differences regarding the age. - Sleep disorders
Background-Aim. Although sleep disturbance is a common complaint among patients of all ages, research suggests that older adults are particularly vulnerable. The aim of this retrospective study was to elucidate the influence of age on clinical characteristics and polysomnographic findings of obstructive sleep apnea syndrome (OSAS) between elderly and younger male patients in a Greek population. Methods. 697 male patients with OSAS were examined from December 2001 to August 2011. All subjects underwent an attended overnight polysomnography (PSG). They were divided into two groups: young and middle-aged (<65 years old) and elderly (≥65 years old). We evaluated the severity of OSAS, based on apnea-hypopnea index (AHI), and the duration of apnea-hypopnea events, the duration of hypoxemia during total sleep time (TST) and during REM and NREM sleep, and the oxygen saturation in REM and in NREM sleep. Results. PSG studies showed that elderly group had significant higher duration of apnea-hypopnea events, longer hypoxemia in TST and in NREM sleep, as well as lower oxygen saturation in REM and NREM sleep than the younger group. Otherwise, significant correlation between BMI and neck circumference with AHI was observed in both groups. Conclusions. The higher percentages of hypoxemia during sleep and longer duration of apnea-hypopnea events that were observed in the elderly group might be explained by increased propensity for pharyngeal collapse and increased deposition of parapharyngeal fat, which are associated with aging. Another factor that could explain these findings might be a decreased partial arterial pressure of oxygen (PaO2) due to age-related changes in the respiratory system.
Immunohistochemical expression of VEGF, HIF1-a, and PlGF in malignant melanomas and dysplastic nevi. - Melanoma research
We evaluated the role of vascular endothelial growth factor (VEGF), placental growth factor (PlGF), and hypoxia-inducible factor 1-a (HIF1-a) in melanoma angiogenesis and investigated their expression in dysplastic nevi, as potential melanoma precursors. In addition, we examined a possible correlation of VEGF expression with PlGF and HIF1-a. These factors were detected immunohistochemically in 95 melanomas of all types and stages and in 28 dysplastic nevi. We used 10 intradermal melanocytic nevi as controls. HIF1-a was expressed in 93 out of 95 (97.89%) melanomas and in none of the dysplastic or control nevi. HIF1-a expression was more intense in melanocytes around necrotic areas but did not correlate with melanoma type, the Clark staging or the Breslow thickness. A strong positive association was detected between HIF1-a and VEGF expression in all cases. VEGF was detected in 82 out of 95 (86.31%) melanomas and in 21 out of 28 (75%) dysplastic nevi, whereas it was expressed weakly in neoplastic cells of the controls. Its expression was more intense in melanomas, especially in nodular melanomas of elevated stage and thickness. PIGF was detected in 46 out of 95 (48.42%) melanomas and in none of the nevi. Expression did not correlate with melanoma staging nor thickness; however, it was more intense in superficial spreading melanomas, where a weak positive association between VEGF and PlGF was also detected. There was no association between HIF1-a and PlGF in any melanoma type. Hypoxia, through the expression of HIF1-a, plays a key role in melanoma progression; it activates VEGF secretion, which induces angiogenesis and metastasis. The role of PlGF seems to be limited.
Characterization of Molecular Evolution in Multi-Drug Resistant of Mycobacterium tuberculosis by rpoB Gene in Patient with Active Pulmonary Tuberculosis from Iranian Isolates. - International journal of biomedical science : IJBS
This is the first genetic biodiversity study of Mycobacterium tuberculosis in Iran. Thus, we investigated the genetic patterns of strains isolated in the first survey of anti-tuberculosis drug-resistance by rpoB gene as part of the Global Project of Anti-tuberculosis Drug Resistance Surveillance (IAU, Iran). A 411-bp fragment of the rpoB gene, containing the sequence of the 81-bp rpoB fragment, was amplified by PCR and the rpoB gene fragments of tuberculosis strains were sequenced using the Amersham auto sequencer. For analysing tree evolution used method UPGMA and Neighbour-Joining. Clinical isolates (34/163) were analyzed by using sequencing gene rpoB and genotyped by program MEGA. The results were compared with the international database. Multi-drug resistant (MDR) was 14% in never treated patients and 8% in previously treated patients. Mutations in rpoB gene and katG genes were detected in 95% and 84% of the MDR strains, respectively. Two clusters were found to be identical by the four different analysis methods, presumably representing cases of recent transmission of MDR tuberculosis. The other strains are divided into 2 groups: group A - similar to the standard and Eastern strains (China, Taiwan) and group B - strains of another genotype. They are grouped separately on the dendrogram and became prevalent in Iran (they are called Iranian residential strains). This study gives a first overview of the M. tuberculosis strains circulating in Iran during the first survey of anti-tuberculosis drug-resistance. It may aid in the creation of a national database that will be a valuable support for further studies.
Oxidative stress stimulates multiple MAPK signalling pathways and phosphorylation of the small HSP27 in the perfused amphibian heart. - The Journal of experimental biology
We investigated the activation of three subfamilies of MAPKs (ERK, JNKs and p38-MAPK) by oxidative stress in the isolated perfused amphibian heart. Activation of p43-ERK by 100 micro mol l(-1) H(2)O(2) was maximally observed within 5 min, remained elevated for 30 min and was comparable with the effect of 1 micro mol l(-1) PMA. p43-ERK activation by H(2)O(2) was inhibited by PD98059 but not by SB203580. The p46 and p52 species of JNKs were maximally activated by 2.5- and 2.1-fold, respectively, by 100 micro mol l(-1) H(2)O(2) within 2 min. JNK activation was still detectable after 15 min, reaching control values at 30 min of treatment. p38-MAPK was maximally activated by 9.75-fold by 100 micro mol l(-1) H(2)O(2) after 2 min and this activation progressively declined thereafter, reaching control values within 45 min of treatment. The observed dose-dependent profile of p38-MAPK activation by H(2)O(2) revealed that 30 micro mol l(-1) H(2)O(2) induced maximal phosphorylation, whereas 100-300 micro mol l(-1) H(2)O(2) induced considerable activation of the kinase. Our studies also showed that the phosphorylation of MAPKAPK2 by H(2)O(2) followed a parallel time-dependent pattern and that SB203580 abolished this phosphorylation. Furthermore, our experiments clearly showed that 30 micro mol l(-1) H(2)O(2) induced a strong, specific phosphorylation of HSP27. Our immunohistochemical studies showed that immune complexes of phosphorylated forms of both p38-MAPK and HSP27 were strongly enhanced by 30 micro mol l(-1) H(2)O(2) in the perinuclear region as well as dispersedly in the cytoplasm of ventricular cells and that SB203580 abolished this phosphorylation. These data indicate that oxidative stress is a powerful activator of all three MAPK subfamilies in the amphibian heart. Stimulation of p38-MAPK and the consequent phosphorylation of HSP27 may be important in cardioprotection under such conditions.

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