Degree Of Atrophy Research Articles

TREATMENT OF UNDESIRABLE CONSEQUENCES AFTER AESTHETIC BLEPHAROPLASTY

The purpose of the work is to improve the results of postoperative complications of the lower eyelid after blepharoplasty.
 Materials and methods. A retrospective study of 14 patients in the postoperative period after blepharoplasty was conducted. All patients had a diagnosis: Age-related changes in the skin of the upper and lower eyelids (ptosis of the skin of the eyelids) before surgery and after surgery, patients had complications with the diagnosis: Dislocation of the lower eyelid, in the postoperative period. In the early postoperative period (up to 6 months), all patients with complications underwent non-surgical correction. Patients were divided into two groups: 1 group - traditional conservative therapy was used, including massage and administration of a glucocorticosteroid solution, 2 group - author's treatment scheme using an erbium laser (Er: YAG, 20940 nm).
 Results. A retrospective study was conducted and it was proved that the author's scheme using an erbium laser (Er: YAG, 20940 nm) gives positive treatment results. Errors in the diagnosis and planning of the volume of surgery, surgical errors, in our opinion, are the main causes of formidable complications that affect the function of the vision organ. Despite the fact that aesthetic blepharoplasty by many surgeons is considered as the simplest surgical intervention and mastered by novice surgeons in the first place, one should not forget about "pitfalls" and possible dramatic consequences, which are caused by neglect of the nuances and precision of surgical equipment, as well as errors in the diagnosis and planning of the volume of surgery.
 Conclusion. Aesthetic blepharoplasty is an operation that requires the individual approach of highly qualified specialists. To avoid the development of complications, not only the degree of atrophy of the skin of the eyelids, but also the peculiarities of the structure of the eyelids and the periorbital region should be taken into account.

Genetic Factors, Brain Atrophy, and Response to Rehabilitation Therapy After Stroke

Objective Patients show substantial differences in response to rehabilitation therapy after stroke. We hypothesized that specific genetic profiles might explain some of this variance and, secondarily, that genetic factors are related to cerebral atrophy post-stroke. Methods The phase 3 ICARE study examined response to motor rehabilitation therapies. In 216 ICARE enrollees, DNA was analyzed for presence of the BDNF val66met and the ApoE ε4 polymorphism. The relationship of polymorphism status to 12-month change in motor status (Wolf Motor Function Test, WMFT) was examined. Neuroimaging data were also evaluated (n=127). Results Subjects were 61±13 years old (mean±SD) and enrolled 43±22 days post-stroke; 19.7% were BDNF val66met carriers and 29.8% ApoE ε4 carriers. Carrier status for each polymorphism was not associated with WMFT, either at baseline or over 12 months of follow-up. Neuroimaging, acquired 5±11 days post-stroke, showed that BDNF val66met polymorphism carriers had a 1.34-greater degree of cerebral atrophy compared to non-carriers (P=.01). Post hoc analysis found that age of stroke onset was 4.6 years younger in subjects with the ApoE ε4 polymorphism (P=.02). Conclusion Neither the val66met BDNF nor ApoE ε4 polymorphism explained inter-subject differences in response to rehabilitation therapy. The BDNF val66met polymorphism was associated with cerebral atrophy at baseline, echoing findings in healthy subjects, and suggesting an endophenotype. The ApoE ε4 polymorphism was associated with younger age at stroke onset, echoing findings in Alzheimer’s disease and suggesting a common biology. Genetic associations provide insights useful to understanding the biology of outcomes after stroke.

The effect of different doses of octenidine hexafluorosilicate on the development of dental caries in rats

At present, ammonium hexafluorosilicate and hexafluorosilicates of organic amonium cations are actively studied as potential anticaries agents, which demonstrate certain advantages over traditional compounds of fluorine. Previously, it was shown that hexafluorosilicates with bactericidal cations of chlorhexidine, polyhexamethyleneguanidine and cetylpyridinium effectively reduce the number and depth of carious lesions of teeth in rats and at the same time significantly improve the biochemical parameters of the pulp of the teeth.
 The aim of the work – to study the effect of different doses of octenidine hexafluorosilicate (OHFS) on the incidence of dental caries in rats fed a cariogenic diet (CD).
 OHFC preparations were applied to the teeth and gums of rats in the composition of phytogels based on Na-salt of carboxymethylcellulose. In the incisor pulp, the activity of alkaline (ALP) and acidic (ACP) phosphatases, elastase, lysozyme was determined, and the mineralizing index (MI) was calculated. The number and depth of dental caries lesions were calculated and caries prophylactic efficacy (CPE) was calculated. The activity of elastase, catalase, lysozyme and urease was determined in the gums, and the degree of atrophy of the alveolar process was determined.
 Determination of dental caries lesions shows that CD does not increase the number of carious lesions, and after the application of gels with OHFS, their number significantly decreases. The most effective was the concentration of the OHFS gel, equal to 2 mg/ml, although the concentration of the OHFS gel 1 mg/ml showed a decrease by 33.3%. The calculated CPE is 33.3% for a gel with 1 mg/ml OHFS, 36.4% for a gel with 2 mg/ml and 24.2% for a gel with 4 mg/ml. It has been shown that in rats receiving CD, the ALP activity significantly decreases and the ACP activity significantly increases, which gives a significant decrease in MI from 43.9 to 28.9. Application of gels with OHFS returns the activity of both phosphatases to the control level and almost completely normalizes MI, and the concentration of OHFS gel of 2 mg/ml turned out to be the most effective. Application of gels with 1 mg/ml and 2 mg/ml OHFS reduced elastase activity by 6% and 12%, respectively, whereas application of a gel with 4 mg/ml OHFS did not result in a decrease in elastase activity. From the results of determining the degree of dysbiosis in the blood serum of rats, it can be seen that CD causes the development of generalized dysbiosis. Application of gels with OHFS significantly reduce the degree of dysbiosis, especially gels with OHFS concentrations of 1 and 2 mg/ml.
 Oral application of gels containing OHFS reduces the incidence of caries on the teeth, increases the mineralizing activity of the pulp and reduces the degree of generalized dysbiosis. The most effective concentration of the OHFS gel is 2 mg/ml, which corresponds to a dose of 2.2 mg/kg.

Muscle magnetic resonance imaging in myotonic dystrophy type 1 (DM1): Refining muscle involvement and implications for clinical trials.

BackgroundOnly a few studies have reported muscle imaging data on small cohorts of patients with myotonic dystrophy type 1 (DM1). We aimed to investigate the muscle involvement in a large cohort of patients in order to refine the pattern of muscle involvement, to better understand the pathophysiological mechanisms of muscle weakness, and to identify potential imaging biomarkers for disease activity and severity.MethodsOne hundred and thirty‐four DM1 patients underwent a cross‐sectional muscle magnetic resonance imaging (MRI) study. Short tau inversion recovery (STIR) and T1 sequences in the lower and upper body were analyzed. Fat replacement, muscle atrophy and STIR positivity were evaluated using three different scales. Correlations between MRI scores, clinical features and genetic background were investigated.ResultsThe most frequent pattern of muscle involvement in T1 consisted of fat replacement of the tongue, sternocleidomastoideus, paraspinalis, gluteus minimus, distal quadriceps and gastrocnemius medialis. Degree of fat replacement at MRI correlated with clinical severity and disease duration, but not with CTG expansion. Fat replacement was also detected in milder/asymptomatic patients. More than 80% of patients had STIR‐positive signals in muscles. Most DM1 patients also showed a variable degree of muscle atrophy regardless of MRI signs of fat replacement. A subset of patients (20%) showed a ‘marbled’ muscle appearance.ConclusionsMuscle MRI is a sensitive biomarker of disease severity alsofor the milder spectrum of disease. STIR hyperintensity seems to precede fat replacement in T1. Beyond fat replacement, STIR positivity, muscle atrophy and a ‘marbled’ appearance suggest further mechanisms of muscle wasting and weakness in DM1, representing additional outcome measures and therapeutic targets for forthcoming clinical trials.

Variation in muscle and neuromuscular junction morphology between atrophy-resistant and atrophy-prone muscles supports failed re-innervation in aging muscle atrophy.

In advanced age, there is an accelerated decline in skeletal muscle mass that appears to be secondary to repeated cycles of denervation-reinnervation and eventually, failed reinnervation. However, whether variation in reinnervation capacity explains why some muscles are less vulnerable to age-related atrophy has not been addressed. In this study we examined changes in neuromuscular junction (NMJ) morphology, fiber cross-sectional area (CSA) and fiber type, accumulation of severely atrophied myofibers, and expression of a marker of denervation in four muscles that exhibit differences in the degree of age-related atrophy and which span the extremes of fiber type composition in 8 mo old (8M) and 34 mo old (34M) male Fischer 344 Brown Norway F1 hybrid rats. Aging muscle atrophy was most pronounced in the fast twitch gastrocnemius (Gas; 25%) and similar between extensor digitorum longus (EDL) and slow-twitch soleus (Sol) muscle (14-15%), whereas the slow-twitch adductor longus (AL) increased in mass by 21% between 8M and 34M (P<0.05 for all). Only the Sol exhibited significant alterations in fiber type with aging, and there was a decrease in fiber CSA in the Gas, EDL, and Sol (P<0.05) with aging that was not seen in the AL. Muscles that atrophied had an increased fraction of severely atrophic myofibers (P<0.05), but this was not observed in the AL. The Gas and EDL both demonstrated a similar degree of age-related remodeling of pre- and post-synaptic NMJ components. On the other hand, pre- and post-synaptic morphology underwent greater changes with aging in the AL, and many of these same morphological variables were already greater in the Sol vs AL at 8M, suggesting the Sol had already undergone substantial remodeling and may be nearing its adaptive limits. Consistent with this idea, analysis of NMJ morphology in Sol from 3M rats exhibited similar values as 8M AL, and the Sol demonstrated greater expression of the denervation marker neural cell adhesion molecule (NCAM) compared to the AL at 34M. Collectively, our results are consistent with NMJ remodeling capacity being finite with aging and that maintained remodeling potential confers atrophy protection in aging skeletal muscle by reducing the degree of persistent denervation.

What Are the Key Points of Treatment for Cases of Mild Cognitive Impairment? Based on the Evaluation of Cognitive Function Tasks in the ADASJcog

Background/Aims: The aims of this study were to identify the degree of atrophy of the hippocampus in image findings and which cognitive function items should be focused on when treating mild cognitive impairment. Methods: A total of 66 cases with mild cognitive impairment were included in the study over a 1.5-year observation period. MR images were used to assess hippocampal atrophy, and cognitive function was assessed by the ADASJcog test. Results: In the mild dementia group, there was a hierarchical difference in the 4 cognitive impairments in which each degree was significantly higher hierarchically. In the normally improved group, memory and act dysfunction was significantly improved, and in deteriorated cases, memory, orientation, and act dysfunction increased significantly. The normally improved group tended to have lighter hippocampal atrophy than the deteriorating group. Discussion: In early treatment of mild cognitive impairment, it is important to focus on which cognitive items to treat, but there are no reports that present them numerically. Because it is not clear, there may be a risk that dementia may progress due to stunned treatment. It became clear that it was meaningful to show it, and it was the orientation and act function. Conclusion: It was suggested that hippocampal atrophy should be kept within the normal range and that the key treatment was mainly to improve memory and act dysfunction without reducing orientation function.

Neural networks in the predictive diagnosis of cognitive impairment in type 1 and type 2 diabetes mellitus

Cognitive dysfunction, including mild cognitive impairment and dementia, is increasingly recognized as a serious complication of diabetes mellitus (DM) that affects patient well-being and disease management. Magnetic resonance imaging (MRI)-studies have shown varying degrees of cortical atrophy, cerebral infarcts, and deep white matter lesions. To explain the relationship between DM and cognitive decline, several hypotheses have been proposed, based on the variability of glycemia leading to morphometric changes in the brain. The ability to predict cognitive decline even before its clinical development will allow the early prevention of this pathology, as well as to predict the course of the existing pathology and to adjust medication regimens. To create a computer neural network model for predicting the development of cognitive impairment in DM on the basis of brain neuroimaging techniques. The study was performed in accordance with the standards of good clinical practice; the protocol was approved by the Ethics Committee. The study included 85 patients with type 1 diabetes and 95 patients with type 2 diabetes, who were divided into a group of patients with normal cognitive function and a group with cognitive impairment. The patient groups were comparable in age and duration of disease. Cognitive impairment was screened using the Montreal Cognitive Assessment Scale. Data for glycemic variability were obtained using continuous glucose monitoring (iPro2, Libre). A standard MRI scan of the brain was performed axially, sagittally, and coronally on a Signa Creator E, GE Healthcare, 1.5 Tesla, China. For MRI data processing we used Free Surfer program (USA) for analysis and visualization of structural and functional neuroimaging data from cross-sectional or longitudinal studies, and for segmentation we used Recon-all batch program directly. All statistical analyses and data processing were performed using Statistica Statsofi software (version 10) on Windows 7/XP Pro operating systems. The IBM WATSON cognitive system was used to build a neural network model. As a result of the study, cognitive impairment in DM type 1was predominantly of mild degree 36.9% (n=24) and moderate degree 30.76% (n=20), and in DM type 2 mild degree 37% (n=30), moderate degree 49.4% (n=40) and severe degree 13.6% (n=11). Cognitive functions in DM type 1 were impaired in memory and attention, whereas in DM type 2 they were also impaired in tasks of visual-constructive skills, fluency, and abstraction (p0.001). The analysis revealed differences in glycemic variability indices in patients with type 1 and type 2 DM and cognitive impairment. Standard MRI of the brain recorded the presence of white and gray matter changes (gliosis and leukoareosis). General and regional cerebral atrophy is characteristic of type 1 and type 2 DM, which is associated with dysglycemia. When building neural network models for type 1 diabetes, the parameters of decreased volumes of the brain regions determine the development of cognitive impairment by 93.5%, whereas additionally, the coefficients of glycemic variability by 98.5%. The same peculiarity was revealed in type 2 DM 95.3% and 97.9%, respectively. In DM type 1 and type 2 with cognitive impairment, elevated coefficients of glycemic variability are more frequently recorded. This publication describes laboratory and instrumental parameters as potential diagnostic options for effective management of DM and prevention of cognitive impairment. Neural network models using glycemic variability coefficients and MR morphometry allow for predictive diagnosis of cognitive disorders in both types of diabetes.

MRI-based thalamic volumetry in multiple sclerosis using FSL-FIRST: Systematic assessment of common error modes.

FSL's FMRIB's Integrated Registration and Segmentation Tool (FSL-FIRST) is a widely used and well-validated tool. Automated thalamic segmentation is a common application and an important longitudinal measure for multiple sclerosis (MS). However, FSL-FIRST's algorithm is based on shape models derived from non-MS groups. As such, the present study sought to systematically assess common thalamic segmentation errors made by FSL-FIRST on MRIs from people with multiple sclerosis (PwMS). FSL-FIRST was applied to generate thalamic segmentation masks for 890 MR images in PwMS. Images and masks were reviewed systematically to classify and quantify errors, as well as associated anatomical variations and MRI abnormalities. For cases with overt errors (n = 362), thalamic masks were corrected and quantitative volumetric differences were calculated. In the entire quantitative volumetric group, the mean volumetric error of FSL-FIRST was 2.74% (0.360 ml): among only corrected cases, the mean volumetric error was 6.79% (0.894 ml). The average percent volumetric error associated with seven error types, two anatomical variants, and motions artifacts are reported. Additional analyses showed that the presence of motion artifacts or anatomical variations significantly increased the probability of error (χ2 =18.14, p<.01 and χ2 =64.89, p<.001, respectively). Finally, thalamus volume error was negatively associated with degree of atrophy, such that smaller thalami were systematically overestimated (r = -.28, p<.001). In PwMS, FSL-FIRST thalamic segmentation miscalculates thalamic volumetry in a predictable fashion, and may be biased to overestimate highly atrophic thalami. As such, it is recommended that segmentations be reviewed and corrected manually when appropriate for specific studies.

Visualization and Spectral Analysis of Pubic Periosteum Atrophy

The atrophy of the pubic periosteum is developing in patients with a long history of femoral hernia. The traditional plastic surgery methods are efficient only in patients with femoral hernia when the Cooper ligament of the pubic periosteum is preserved. The aim of this study is to determine the thinning and atrophy degree of the pubic periosteum in patients with femoral hernia using computer tomography and Raman spectroscopy analysis. It was shown that thinning of the periosteum due to atrophy is accompanied by a significant change in the hydroxyapatite ν 1 PO 4 and Amide I (959/1660 cm –1 ) Raman peaks ratio and decrease in the 1070/959 cm –1 peaks. It was found that Raman spectroscopy is able to confirm the preservation and atrophy degree of the pubic periosteum during surgical resection with an 83% accuracy.

No effects of early functional mobilization on gait patterns after acute Achilles tendon rupture repair.

This study aimed to compare recovery of gait patterns in patients treated with early functional mobilization (EFM) or standard treatment (ST) after Achilles tendon rupture repair. Second, this study aimed to explore associations between gait patterns and tendon elongation and calf muscle atrophy, respectively. Forty-seven patients (12 females), mean age 38.7 (7.3) years, were included. Patients were postoperatively randomized to EFM (n = 29), including immediate weightbearing and ankle motion for 6 weeks, or ST (n = 18), with 2 weeks of unloading in a plaster cast followed by 4 weeks of weightbearing in an orthosis. Three-dimensional gait analyses were performed at 8 weeks and 6 months postoperatively to evaluate ankle and knee kinematics and kinetics. Ultrasound imaging was performed to assess tendon length and calf muscle atrophy. At 8 weeks, there were no significant group differences in ankle and knee kinematics and kinetics, while side-to-side differences between injured and uninjured side were present within both groups. At 6 months, the ST group exhibited higher generating ankle power and greater peak moments in ankle and knee compared to the EFM group. In both groups, peak ankle dorsiflexion angle was greater on the injured side compared to the uninjured side. No correlations were found between ankle joint gait deviations and degree of tendon elongation or muscle atrophy. Clinical significance: The accelerated rehabilitation regimen with EFM did not result in a more symmetrical gait pattern. The gait pattern deviations in the ankle joint were not related to the degree of muscle atrophy or tendon elongation.

Brain atrophy and endovascular treatment effect in acute ischemic stroke: a secondary analysis of the MR CLEAN trial.

BackgroundBrain atrophy is suggested to impair the potential for functional recovery after acute ischemic stroke. We assessed whether the effect of endovascular treatment is modified by brain atrophy in patients with acute ischemic stroke due to large vessel occlusion.MethodsWe used data from MR CLEAN, a multicenter trial including patients with acute ischemic stroke due to anterior circulation large vessel occlusion randomized to endovascular treatment plus medical care (intervention) versus medical care alone (control). We segmented total brain volume (TBV) and intracranial volume (ICV) on baseline non-contrast computed tomography (n = 410). Next, we determined the degree of atrophy as the proportion of brain volume in relation to head size (1 − TBV/ICV) × 100%, analyzed as continuous variable and in tertiles. The primary outcome was a shift towards better functional outcome on the modified Rankin Scale expressed as adjusted common odds ratio. Treatment effect modification was tested using an interaction term between brain atrophy (as continuous variable) and treatment allocation.ResultsWe found that brain atrophy significantly modified the effect of endovascular treatment on functional outcome (P for interaction = 0.04). Endovascular treatment led to larger shifts towards better functional outcome in the higher compared to the lower range of atrophy (adjusted common odds ratio, 1.86 [95% CI: 0.97–3.56] in the lowest tertile vs. 1.97 [95% CI: 1.03–3.74] in the middle tertile vs. 3.15 [95% CI: 1.59–6.24] in the highest tertile).ConclusionBenefit of endovascular treatment is larger in the higher compared to the lower range of atrophy, demonstrating that advanced atrophy should not be used as an argument to withhold endovascular treatment.

The Effects of Sex and Body Weight on Renal Graft Function-The Role of CCL2.

There are reports on the effects of excessive recipient body weight on renal graft function. Increased CCL2 (chemokine CC-mortif ligand 2) production is observed in patients with excessive body weight. CCL2 also exacerbates the inflammatory process in the renal graft. A total of 49 renal graft recipients of both sexes having undergone renal biopsy within the last 18 months were retrospectively reviewed. At their most recent appointment the patients’ plasma concentrations of CCL2 were evaluated. Renal function was assessed retrospectively. CCL2 concentrations were higher in men than women (p < 0.047), while higher CCL2 levels were associated with a decrease in eGFR (estimated glomerular filtration rate) during the first year post Tx (kidney transplantation). CCL2 negatively correlated with eGFR at 5 years (R = −0.45, p < 0.040997) and positively correlated with the degree of tubular atrophy in renal biopsy specimens (R = 0.43, p < 0.027293) and with systolic pressure. Men showed significantly higher BMI (body mass index) values at the time of Tx and at their last appointment than women did (p < 0.000403; p < 0.000613, respectively). Men showed poorer long-term renal graft function, with significantly lower eGFR values at 4 and 5 years into the post-transplantation period. The male sex and excessive body weight have adverse effects on short- and long-term renal graft function, which is associated with increased levels of CCL2.

Erythropoietin improves effects of mesenchymal stem cells in an experimental model of sepsis

In the last years several studies have shown that mesenchymal stem cells (MSCs) are able to reduce the systemic inflammatory response and mortality in experimental models of sepsis. As recently found, the surface of MSCs have receptors for erythropoietin (EPO). So we hypothesized that the introduction of EPO together with MSCs may enhance their effect and improve the results of sepsis treatment.&#x0D; Aim: То evaluate morphologic and immunologic effects of combined treatment with EPO and MSC in an experimental LPS sepsis model in rats.&#x0D; Methods: 50 Wistar rats were randomized into 5 groups: Group 1 - the healthy controls, Groups 2-5 were intraperitoneally introduced bacterial LPS 20 mg/kg. Two hours after LPS injection animals received the following intravenous treatments: Group 3 - 4xl05 allogeneic MSCs, Group 4 - 8.5 pg of recombinant EPO-beta, Group 5 - MSCs and EPO in the same doses. Surviving animals were euthanased on the 4th day. The morphological study of the liver, spleen, thymus, lungs, kidney tissues was performed. We analyzed the tissue changes, white blood cells count and serum level of IL-l, IL-2, IL-6, TNF-.&#x0D; Results: Mortality in LPS groups did not differ. The highest white blood cells count was found in the group of combined treatment EPO+MSCs (8.15x106 cells/ml) compared with controls (2,15x10s cells/ml) and LPS controls (6,52x10s cells/ml). There were no differences in levels of TNF-, IL-2 and IL-6 between the groups, but serum IL-1 level in groups 2 and 4 was significantly higher than in treated with MSCs and MSCc + EPO animals. Histologically in the group 5 we observed significantly less leukocyte lung interalveolar septal infiltration and kidney tubular dystrophy. The most significant differences in group LPS + EPO were found in the lymphoid tissue - considerable hyperplasia of spleen white pulp and thymus cortex, whereas in the other groups different degrees of atrophy of the corresponding zones were noted.&#x0D; Conclusions: Combined treatment with EPO and MSCs can reduce acute lung injury and kidney damage, cause hyperplasia of lymphoid tissue and enhance the immune response more than separate treatment in an experimental model of sepsis in rats.

Ultrastructural study of the lacrimal glands in severe dry eye disease following Stevens-Johnson syndrome

PurposeThis study aimed to examine the ultrastructural features of the lacrimal glands of patients with severe dry eye due to Stevens-Johnson syndrome (SJS). MethodsBiopsies form orbital lobes of six lacrimal glands obtained from fresh body donors (n=3) and patients with SJS (n=3; absolute tear deficiency; 2-6 months of disease duration) were examined using transmission electron microscopy (TEM). ResultsOn TEM, normal lacrimal glandular tissue shows columnar acinar epithelial cells containing basally located rounded or oval euchromatic nuclei with cytoplasmic electron dense and ­moderately electron-dense secretory granules. Histologically, the lacrimal gland biopsies showed varied degree of acinar atrophy with lymphocytic infiltration in SJS patients. While on TEM, the lacrimal glands in SJS patients showed homogenous appearance of the nuclear chromatin of acinar cells with no differentiation into hetero-or euchromatin and loss of nucleoli. The cytoplasm lacked any electron dense material and showed significant loss of endoplasmic reticulum, mitochondria and Golgi bodies. The myoepithelial cells shared similar characteristics as in acinar epithelial cells along with loss of spindle shaped processes. ConclusionTransmission electron microscopy revealed ultrastructural changes in terms of nuclear composition, secretory vesicles, lysosomal vacuolation and myoepithelial cell distribution in the lacrimal glands of SJS patients.

Influence of direct prostheses on the condition of the alveolar processes during dental implantation

ObjectiveThe purpose of this article is to study of the processes accompanying osseointegration of the dental implants using various plate prostheses as temporary constructions, as well as to compare the dynamics of changes in the state of the jaw alveolar processes. Materials and methodsThe effect of dentures on the condition of the alveolar processes was studied in all patients according to the technique developed by L. Chulak on the 7th, 14th, 30th day and in 3, 6 months. To verify the results, the degree of atrophy of the alveolar processes was also determined by the second method the authors have chosen at the same time as indicated above. ResultsThe measurement results confirm linear changes in the height of the alveolar processes of the jaws with a decrease in the tissues of the prosthetic area. Throughout the duration of the examination, atrophy of the tissues of the alveolar processes is observed. Judging by the results obtained during the patients’ study, it can be concluded that when applied as a temporary prosthesis with a dental delayed implantation of a partial denture made of polypropylene, the results of the state of the hard tissues of the mandible alveolar process show a better adaptation of the mucous membrane and slowing of atrophy of the jaw alveolar processes with this type of prosthetics.

548 - Cognitive aging and cognitive reserve

IntroductionThe aging processes are accelerating in all regions of the world. The involvement of older people in production and social processes determines the need to maintain a high level of social and psychological adaptation, despite the progressive pathology of the brain caused by its aging. This increases the relevance of research related to the study of biological reserves of the brain and psychological and social mechanisms of human adaptation in late adulthood. The risk of developing cognitive disorders is not fatal. According to some observations, even in the hippocampal type of UKR, despite the content of amyloid in the brain, the functional and social activity of the elderly remains high. Prospective studies show that people with high cognitive reserve have a lower risk of developing dementia. Cognitive reserve is the brain’s resistance to damage. Cognitive reserve is the ability of the brain to cope with the consequences of damage caused by external influences, brain stroke, chronic brain ischemia, neurodegenerative diseases, and age-related changes. Cognitive reserve is the brain’s ability to functionally compensate for and minimize clinical manifestations of cognitive impairment. The mechanisms of cognitive reserve in normal and Alzheimer’s disease are different. In healthy older adults, a higher cognitive reserve correlates with larger brain sizes and effective strategies for performing cognitive tasks. In the early stages of Alzheimer’s disease and Alzheimer’s disease, the size of the brain decreases. But high brain activity helps preserve cognitive resources. Excessive brain activity in dementia is a compensatory mechanism. This is confirmed by the results of functional magnetic resonance imaging of the brain. Of course, the degree of brain atrophy is a predisposing factor for dementia, but it is not a mandatory factor for cognitive decline. So, the symptoms of dementia do not appear until you have crossed the critical border of damage to the brain substance. Progressive brain atrophy underlies the clinical manifestations of dementia in neurodegenerative diseases, but the correlation between the degree of brain damage and cognitive impairment is not linear.Research materials and methodsAn observational 10-year longitudinal study was conducted. In 2006, moderate cognitive impairment was found in 66 patients. The group of patients included 49 women and 49 men. Their average age in 2006 was 59.3±5.2 years. In 2006, the severity of cognitive decline was 26.2±1.9 points on the MMSE scale. This corresponds to indicators of moderate cognitive impairment. Research methods: clinical and psychopathological, psychometric, statistical. Questionnaire “Loss and acquisition of personal resources” (N. Vodopyanova, M. Stein), MMSE scale.Research resultIn 2006, amyloid was detected in the spinal fluid of all patients selected for the study group. If a patient developed dementia, they were given specific therapy. The dynamics of cognitive functions in patients was different. Mild dementia was formed in 53% of patients. Moderate dementia was formed in 10.6% of patients. Moderate cognitive impairment (pre-dementia) persisted in 36.4% of patients. Hereditary burden of dementia in patients with moderate dementia was detected 2 times more often. Back in 2006, we identified the leading sensory systems of patients. The master sensor system determines the modality of the main information flow. This is the most important part of the information that a person interacts with. This is the basis of interaction with reality. This is the basis of cognitive functions. Correlations of age-specific lesions of the corresponding sensory systems with the severity of cognitive decline were found in patients with the corresponding sensory modality (Spearman’s Correlation Coefficient-r, p&lt;0.05): presbyacoussis – auditory r=0.667, presbyopia-visual r=0.705. The influence of psychosocial factors on the condition of patients was studied. In dementia, significant history of psychotrauma was found in 35.7%. Moderate stress was detected in the group of patients with moderate cognitive impairment in 33.3%. Moderate stress was detected in the group of patients with dementia in 83.3%. Stress of loss of life meaning was detected more often in patients with dementia 76.7%. It is important not only what stresses a person endures, but how they can cope with them. Dementia patients were statistically more likely to have unproductive coping strategies that did not help them cope adequately with stress.ConclusionsThe concept of cognitive reserve suggests possible causes of heterogeneity in the dynamics of cognitive decline in the initial stages of atrophic-degenerative brain diseases: biological causes and psychosocial causes. The concept of cognitive reserve helps to study and develop individual programs for the prevention of severe cognitive disorders.

Clinical study of central cholinergic pathway damage in two mild cognitive impairment patients

ObjectivesTo explore the role of the central cholinergic system in amnestic mild cognitive impairment (aMCI) and mild vascular cognitive impairment (vMCI).MethodsTwenty-five aMCI patients and 25 vMCI patients were enrolled in this study, and 25 healthy people were chosen as a control group. All participants performed a set of cognitive function scales and were subjected to a brain MRI. We analyzed differences in neuropsychological damage between groups, as well as the degree of brain atrophy and changes in the microstructure of central cholinergic pathways (CCP) in relation to effects on neuropsychological scores.Results(1) Regarding neuropsychological characteristics of the three groups, scores on the MoCA scale, immediate memory, delayed recall, cued recall, long time prolonged recognition, and CDR-SB of the control group were significantly better than those of the aMCI and vMCI groups. Scores on immediate memory, delayed memory, cued recall, long time delayed recognition, and Forward of Digital Span Test (FDST) in the aMCI group were lower than those in the vMCI group. Compared with the aMCI group, the vMCI group was significantly delayed in Trail Making Test (TMA)-A, TMT-B, and TMT B-A. There were no significant differences in HAMA, HAMD, MMSE, MoCA, the Boston Naming Test (BNT), language fluency or visual scale of posterior atrophy (Koedam score) between the vMCI and aMCI groups. (2) As for microstructure changes in the central cholinergic pathway, vMCI group had a decreased FA value in the cingulum (Cing) of the medial pathway, but an increased MD value in the external capsule (Excap) of the lateral pathway when compared to other two groups. Furthermore, the CingMD value of the vMCI group was higher than that of the control group, but the difference was not obvious when compared to the aMCI group. (3) Last, we researched microstructural changes to CCP, degree of brain atrophy, and neuropsychological scores by using partial correlation analysis for all participants. CingFA was negatively correlated with TMT-B, B-A, and FDST. CingMD was negatively correlated with FDST. ExcapFA was positively correlated with MMSE and Backward of BDST, while ExcapMD was negatively correlated with MMSE and MoCA. Claustrum (Claus)FA was positively related to MoCA and FDST, but was negatively related to TMT-A. ClausMD was negatively correlated with MoCA and language fluency. Koedam score was positively correlated with CDR-SB, ExcapMD, and ClausMD, but negatively correlated with MMSE score and inverse BDST.ConclusionThe central cholinergic system is involved in the cognitive impairment of both aMCI and vMCI, and their mechanisms may be distinct. aMCI patients may present with primary CCP impairment while vMCI patients probably exhibit impairment secondary to vasogenic damage to the cholinergic system projection network. The lateral cholinergic pathway was more severely impaired than the medial pathway in vMCI patients, in addition to being associated with decreased executive and general cognitive functions. The damage to CCP was related to the degree of brain atrophy, and both may be involved in the development and progression of cognitive dysfunction.

Diminishment of Nrf2 Antioxidative Defense Aggravates Nephrotoxicity of Melamine and Oxalate Coexposure.

Chronic kidney disease (CKD) usually causes devastating healthy impacts on patients. However, the causes affecting the decline of kidney function are not fully revealed, especially the involvement of environmental pollutants. We have revealed that exposure to melamine, a ubiquitous chemical in daily life, is linked to adverse kidney outcomes. Hyperoxaluria that results from exposure to excessive oxalate, a potentially nephrotoxic terminal metabolite, is reportedly associated with CKD. Thus, we explored whether interaction of these two potential nephrotoxicants could enhance kidney injury. We established a renal proximal tubular HK-2 cell model and a Sprague–Dawley rat model of coexposure to melamine with sodium oxalate or hydroxy-L-proline to investigate the interacting adverse effects on kidneys. Melamine and oxalate coexposure enhanced the levels of reactive oxygen species, lipid peroxidation and oxidative DNA damage in the HK-2 cells and kidney tissues. The degrees of tubular cell apoptosis, tubular atrophy, and interstitial fibrosis were elevated under the coexposed condition, which may result from the diminishment of Nrf2 antioxidative capacity. To conclude, melamine and oxalate coexposure aggravates renal tubular injury via impairment of antioxidants. Accumulative harmful effects of exposure to multiple environmental nephrotoxicants should be carefully investigated in the etiology of CKD progression.

Pathologic characterization of canine multiple system degeneration in the Ibizan hound.

Canine multiple system degeneration (CMSD) is a progressive hereditary neurodegenerative disorder commonly characterized by neuronal degeneration and loss in the cerebellum, olivary nuclei, substantia nigra, and caudate nuclei. In this article, we describe 3 cases of CMSD in Ibizan hounds. All patients exhibited marked cerebellar ataxia and had cerebellar atrophy on magnetic resonance imaging. At necropsy, all cases showed varying degrees of cerebellar atrophy, and 2 cases had gross cavitation of the caudate nuclei. Histologic findings included severe degeneration and loss of all layers of the cerebellum and neuronal loss and degeneration within the olivary nuclei, substantia nigra, and caudate nuclei. Pedigree analysis indicated an autosomal recessive mode of inheritance, but the causative gene in this breed is yet to be identified. CMSD resembles human multiple system atrophy and warrants further investigation.

Cortical and Subcortical Brain Area Atrophy in SCA1 and SCA2 Patients in India: The Structural MRI Underpinnings and Correlative Insight Among the Atrophy and Disease Attributes.

Genetically defined spinocerebellar ataxia (SCA) type 1 and 2 patients have differential clinical profile along with probable distinctive cortical and subcortical neurodegeneration. We compared the degree of brain atrophy in the two subtypes with their phenotypic and genotypic parameters. MRI was performed using a 3T scanner (Philips, Achieva) to obtain 3D T1-weighted scans of the whole brain and analyzed by FreeSurfer (version 5.3 and 6 dev.) software. Genetically proven SCA1 (n = 18) and SCA2 (n = 25) patients with age-matched healthy controls (n = 8) were recruited. Clinical severity was assessed by the International Cooperative Ataxia Rating Scale (ICARS). To know the differential pattern of atrophy, the groups were compared using ANOVA/Kruskal-Wallis test and followed by correlation analysis with multiple corrections. Further, machine learning-based classification of SCA subtypes was carried out. We found (i) bilateral frontal, parietal, temporal, and occipital atrophy in SCA1 and SCA2 patients; (ii) reduced volume of cerebellum, regions of brain stem, basal ganglia along with the certain subcortical areas such as hippocampus, amygdala, thalamus, diencephalon, and corpus callosum in SCA1 and SCA2 subtypes; (iii) higher subcortical atrophy SCA2 than SCA1 (iv) correlation between brain atrophy and disease attributes; (v) differential predictive pattern of two SCA subtypes using machine learning approach. The present study suggests that SCA1 and SCA2 do not differ in cortical thinning while a characteristic pattern of subcortical atrophy SCA2 > SCA1 is observed along with correlation of brain atrophy and disease attributes. This may provide the diagnostic guidance of MRI to SCA subtypes and differential therapies.