Recognition of Cytokeratin 18 Marker by Flow Cytometry of Nucleus Pulposus Cells in Human Intervertebral Disc and Comparison of Proliferation and Morphology of these Cells in Chitosan-Gelatin and Alginate Scaffolds

Background: Low back pain is a major economical and social problem nowadays. Intervertebral disc herniation and central degeneration of disc are two major reasons of low back pain that occur because of structural impairment of discs. Intervertebral disc includes the annulus fibrosus, transitional region, and nucleus pulposus (NP). NP forms the central nucleus of the disc. Reduction of cell count and extracellular matrix, especially in NP, causes disc degeneration. Different scaffolds (natural and synthetic) have been used for tissue repairing and regeneration of intervertebral disc in tissue engineering. Most scaffolds have biodegradable and biocompatible characteristics and also prepare a fine condition for proliferation and migration of cells. Although no specific marker or method has been suggested for recognition of NP cells, some studies have used real time and immunocytochemical methods and reported high expression of cytokeratin 19, 18, 8, and others as markers for NP cells. This study aimed to recognize NP cells of human intervertebral disc by flow cytometry of cytokeratin 18 marker. It also compared the proliferation and morphology of these cells in chitosan-gelatin scaffold and alginate scaffold. Methods: NP cells were derived by enzymatic hydrolysis of collagenase from NP tissue of patients undergoing open surgery for discectomy in Alzahra Hospital (Isfahan, Iran). Chitosan was blended with gelatin and glutaraldehyde was used for cross linking of the two polymers. Then, alginate scaffold was prepared. After approving the NP cells by flow cytometry of cytokeratin 18 marker, a cellular suspension with 4 × 105 cells was transferred to each scaffold and cultured for 21 days. Cell viability and proliferation were investigated by trypan blue and methyl thiazolyl tetrazolium (MTT) assay. A scanning electron microscope (SEM) was used to assert the porosity and to survey the structures of the scaffolds. Findings: We can use flow cytometry of cytokeratin 18 markers for recognition of NP cells. MTT assay demonstrated that cell viability on the third day had significant difference with the first day in both scaffolds. There was also a significant reduction in cellular viability from day 3 to day 21. Results of cell count showed that mean difference between cell counts in alginate scaffold was significantly more than chitosan-gelatin scaffold (P < 0.001). Conclusion: Flow cytometry of cytokeratin 18 can be used as a method for recognition of NP cells. Compared to chitosan-gelatin scaffold, alginate scaffold prepared a better condition for proliferation of NP cells. The results of this study suggested that alginate scaffold could be useful in in-vivo studies and treatment

Recognition of Cytokeratin 18 Marker by Flow Cytometry of Nucleus Pulposus Cells in Human Intervertebral Disc and Comparison of Proliferation and Morphology of these Cells in Chitosan-Gelatin and Alginate Scaffolds.

Background: Low back pain is a major economical and social problem nowadays. Intervertebral disc herniation and central degeneration of disc are two major reasons of low back pain that occur because of structural impairment of discs. Intervertebral disc includes the annulus fibrosus, transitional region, and nucleus pulposus (NP). NP forms the central nucleus of the disc. Reduction of cell count and extracellular matrix, especially in NP, causes disc degeneration. Different scaffolds (natural and synthetic) have been used for tissue repairing and regeneration of intervertebral disc in tissue engineering. Most scaffolds have biodegradable and biocompatible characteristics and also prepare a fine condition for proliferation and migration of cells. Although no specific marker or method has been suggested for recognition of NP cells, some studies have used real time and immunocytochemical methods and reported high expression of cytokeratin 19, 18, 8, and others as markers for NP cells. This study aimed to recognize NP cells of human intervertebral disc by flow cytometry of cytokeratin 18 marker. It also compared the proliferation and morphology of these cells in chitosan-gelatin scaffold and alginate scaffold. Methods: NP cells were derived by enzymatic hydrolysis of collagenase from NP tissue of patients undergoing open surgery for discectomy in Alzahra Hospital (Isfahan, Iran). Chitosan was blended with gelatin and glutaraldehyde was used for cross linking of the two polymers. Then, alginate scaffold was prepared. After approving the NP cells by flow cytometry of cytokeratin 18 marker, a cellular suspension with 4 × 105 cells was transferred to each scaffold and cultured for 21 days. Cell viability and proliferation were investigated by trypan blue and methyl thiazolyl tetrazolium (MTT) assay. A scanning electron microscope (SEM) was used to assert the porosity and to survey the structures of the scaffolds. Findings: We can use flow cytometry of cytokeratin 18 markers for recognition of NP cells. MTT assay demonstrated that cell viability on the third day had significant difference with the first day in both scaffolds. There was also a significant reduction in cellular viability from day 3 to day 21. Results of cell count showed that mean difference between cell counts in alginate scaffold was significantly more than chitosan-gelatin scaffold (P < 0.001). Conclusion: Flow cytometry of cytokeratin 18 can be used as a method for recognition of NP cells. Compared to chitosan-gelatin scaffold, alginate scaffold prepared a better condition for proliferation of NP cells. The results of this study suggested that alginate scaffold could be useful in in-vivo studies and treatment

Global, regional, and national burden of neurological disorders, 1990–2016 : a systematic analysis for the Global Burden of Disease Study 2016

Background: Neurological disorders are increasingly recognised as major causes of death and disability worldwide. The aim of this analysis from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016 is to provide the most comprehensive and up-to-date estimates of the global, regional, and national burden from neurological disorders. Methods: We estimated prevalence, incidence, deaths, and disability-adjusted life-years (DALYs; the sum of years of life lost [YLLs] and years lived with disability [YLDs]) by age and sex for 15 neurological disorder categories (tetanus, meningitis, encephalitis, stroke, brain and other CNS cancers, traumatic brain injury, spinal cord injury, Alzheimer's disease and other dementias, Parkinson's disease, multiple sclerosis, motor neuron diseases, idiopathic epilepsy, migraine, tension-type headache, and a residual category for other less common neurological disorders) in 195 countries from 1990 to 2016. DisMod-MR 2.1, a Bayesian meta-regression tool, was the main method of estimation of prevalence and incidence, and the Cause of Death Ensemble model (CODEm) was used for mortality estimation. We quantified the contribution of 84 risks and combinations of risk to the disease estimates for the 15 neurological disorder categories using the GBD comparative risk assessment approach. Findings: Globally, in 2016, neurological disorders were the leading cause of DALYs (276 million [95% UI 247–308]) and second leading cause of deaths (9·0 million [8·8–9·4]). The absolute number of deaths and DALYs from all neurological disorders combined increased (deaths by 39% [34–44] and DALYs by 15% [9–21]) whereas their age-standardised rates decreased (deaths by 28% [26–30] and DALYs by 27% [24–31]) between 1990 and 2016. The only neurological disorders that had a decrease in rates and absolute numbers of deaths and DALYs were tetanus, meningitis, and encephalitis. The four largest contributors of neurological DALYs were stroke (42·2% [38·6–46·1]), migraine (16·3% [11·7–20·8]), Alzheimer's and other dementias (10·4% [9·0–12·1]), and meningitis (7·9% [6·6–10·4]). For the combined neurological disorders, age-standardised DALY rates were significantly higher in males than in females (male-to-female ratio 1·12 [1·05–1·20]), but migraine, multiple sclerosis, and tension-type headache were more common and caused more burden in females, with male-to-female ratios of less than 0·7. The 84 risks quantified in GBD explain less than 10% of neurological disorder DALY burdens, except stroke, for which 88·8% (86·5–90·9) of DALYs are attributable to risk factors, and to a lesser extent Alzheimer's disease and other dementias (22·3% [11·8–35·1] of DALYs are risk attributable) and idiopathic epilepsy (14·1% [10·8–17·5] of DALYs are risk attributable). Interpretation: Globally, the burden of neurological disorders, as measured by the absolute number of DALYs, continues to increase. As populations are growing and ageing, and the prevalence of major disabling neurological disorders steeply increases with age, governments will face increasing demand for treatment, rehabilitation, and support services for neurological disorders. The scarcity of established modifiable risks for most of the neurological burden demonstrates that new knowledge is required to develop effective prevention and treatment strategies. Funding: Bill & Melinda Gates Foundation

Erratum: Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks for 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017

Interpretation: By quantifying levels and trends in exposures to risk factors and the resulting disease burden, this assessment offers insight into where past policy and programme efforts might have been successful and highlights current priorities for public health action. Decreases in behavioural, environmental, and occupational risks have largely offset the effects of population growth and ageing, in relation to trends in absolute burden. Conversely, the combination of increasing metabolic risks and population ageing will probably continue to drive the increasing trends in non-communicable diseases at the global level, which presents both a public health challenge and opportunity. We see considerable spatiotemporal heterogeneity in levels of risk exposure and risk-attributable burden. Although levels of development underlie some of this heterogeneity, O/E ratios show risks for which countries are overperforming or underperforming relative to their level of development. As such, these ratios provide a benchmarking tool to help to focus local decision making. Our findings reinforce the importance of both risk exposure monitoring and epidemiological research to assess causal connections between risks and health outcomes, and they highlight the usefulness of the GBD study in synthesising data to draw comprehensive and robust conclusions that help to inform good policy and strategic health planning

Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks for 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017

Background The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 comparative risk assessment (CRA) is a comprehensive approach to risk factor quantification that offers a useful tool for synthesising evidence on risks and risk–outcome associations. With each annual GBD study, we update the GBD CRA to incorporate improved methods, new risks and risk–outcome pairs, and new data on risk exposure levels and risk–outcome associations. Methods We used the CRA framework developed for previous iterations of GBD to estimate levels and trends in exposure, attributable deaths, and attributable disability-adjusted life-years (DALYs), by age group, sex, year, and location for 84 behavioural, environmental and occupational, and metabolic risks or groups of risks from 1990 to 2017. This study included 476 risk–outcome pairs that met the GBD study criteria for convincing or probable evidence of causation. We extracted relative risk and exposure estimates from 46 749 randomised controlled trials, cohort studies, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. Using the counterfactual scenario of theoretical minimum risk exposure level (TMREL), we estimated the portion of deaths and DALYs that could be attributed to a given risk. We explored the relationship between development and risk exposure by modelling the relationship between the Socio-demographic Index (SDI) and risk-weighted exposure prevalence and estimated expected levels of exposure and risk-attributable burden by SDI. Finally, we explored temporal changes in risk-attributable DALYs by decomposing those changes into six main component drivers of change as follows: (1) population growth; (2) changes in population age structures; (3) changes in exposure to environmental and occupational risks; (4) changes in exposure to behavioural risks; (5) changes in exposure to metabolic risks; and (6) changes due to all other factors, approximated as the risk-deleted death and DALY rates, where the risk-deleted rate is the rate that would be observed had we reduced the exposure levels to the TMREL for all risk factors included in GBD 2017. Findings In 2017, 34·1 million (95% uncertainty interval [UI] 33·3–35·0) deaths and 1·21 billion (1·14–1·28) DALYs were attributable to GBD risk factors. Globally, 61·0% (59·6–62·4) of deaths and 48·3% (46·3–50·2) of DALYs were attributed to the GBD 2017 risk factors. When ranked by risk-attributable DALYs, high systolic blood pressure (SBP) was the leading risk factor, accounting for 10·4 million (9·39–11·5) deaths and 218 million (198–237) DALYs, followed by smoking (7·10 million [6·83–7·37] deaths and 182 million [173–193] DALYs), high fasting plasma glucose (6·53 million [5·23–8·23] deaths and 171 million [144–201] DALYs), high body-mass index (BMI; 4·72 million [2·99–6·70] deaths and 148 million [98·6–202] DALYs), and short gestation for birthweight (1·43 million [1·36–1·51] deaths and 139 million [131–147] DALYs). In total, risk-attributable DALYs declined by 4·9% (3·3–6·5) between 2007 and 2017. In the absence of demographic changes (ie, population growth and ageing), changes in risk exposure and risk-deleted DALYs would have led to a 23·5% decline in DALYs during that period. Conversely, in the absence of changes in risk exposure and risk-deleted DALYs, demographic changes would have led to an 18·6% increase in DALYs during that period. The ratios of observed risk exposure levels to exposure levels expected based on SDI (O/E ratios) increased globally for unsafe drinking water and household air pollution between 1990 and 2017. This result suggests that development is occurring more rapidly than are changes in the underlying risk structure in a population. Conversely, nearly universal declines in O/E ratios for smoking and alcohol use indicate that, for a given SDI, exposure to these risks is declining. In 2017, the leading Level 4 risk factor for age-standardised DALY rates was high SBP in four super-regions: central Europe, eastern Europe, and central Asia; north Africa and Middle East; south Asia; and southeast Asia, east Asia, and Oceania. The leading risk factor in the high-income super-region was smoking, in Latin America and Caribbean was high BMI, and in sub-Saharan Africa was unsafe sex. O/E ratios for unsafe sex in sub-Saharan Africa were notably high, and those for alcohol use in north Africa and the Middle East were notably low. Interpretation By quantifying levels and trends in exposures to risk factors and the resulting disease burden, this assessment offers insight into where past policy and programme efforts might have been successful and highlights current priorities for public health action. Decreases in behavioural, environmental, and occupational risks have largely offset the effects of population growth and ageing, in relation to trends in absolute burden. Conversely, the combination of increasing metabolic risks and population ageing will probably continue to drive the increasing trends in non-communicable diseases at the global level, which presents both a public health challenge and opportunity. We see considerable spatiotemporal heterogeneity in levels of risk exposure and risk-attributable burden. Although levels of development underlie some of this heterogeneity, O/E ratios show risks for which countries are overperforming or underperforming relative to their level of development. As such, these ratios provide a benchmarking tool to help to focus local decision making. Our findings reinforce the importance of both risk exposure monitoring and epidemiological research to assess causal connections between risks and health outcomes, and they highlight the usefulness of the GBD study in synthesising data to draw comprehensive and robust conclusions that help to inform good policy and strategic health planning

Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks for 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017.

BACKGROUND: The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 comparative risk assessment (CRA) is a comprehensive approach to risk factor quantification that offers a useful tool for synthesising evidence on risks and risk-outcome associations. With each annual GBD study, we update the GBD CRA to incorporate improved methods, new risks and risk-outcome pairs, and new data on risk exposure levels and risk-outcome associations. METHODS: We used the CRA framework developed for previous iterations of GBD to estimate levels and trends in exposure, attributable deaths, and attributable disability-adjusted life-years (DALYs), by age group, sex, year, and location for 84 behavioural, environmental and occupational, and metabolic risks or groups of risks from 1990 to 2017. This study included 476 risk-outcome pairs that met the GBD study criteria for convincing or probable evidence of causation. We extracted relative risk and exposure estimates from 46 749 randomised controlled trials, cohort studies, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. Using the counterfactual scenario of theoretical minimum risk exposure level (TMREL), we estimated the portion of deaths and DALYs that could be attributed to a given risk. We explored the relationship between development and risk exposure by modelling the relationship between the Socio-demographic Index (SDI) and risk-weighted exposure prevalence and estimated expected levels of exposure and risk-attributable burden by SDI. Finally, we explored temporal changes in risk-attributable DALYs by decomposing those changes into six main component drivers of change as follows: (1) population growth; (2) changes in population age structures; (3) changes in exposure to environmental and occupational risks; (4) changes in exposure to behavioural risks; (5) changes in exposure to metabolic risks; and (6) changes due to all other factors, approximated as the risk-deleted death and DALY rates, where the risk-deleted rate is the rate that would be observed had we reduced the exposure levels to the TMREL for all risk factors included in GBD 2017

Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks for 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017

Stanaway JD, Afshin A, Gakidou E, et al. Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks for 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2018;392(10159):1923-1994.Background The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 comparative risk assessment (CRA) is a comprehensive approach to risk factor quantification that offers a useful tool for synthesising evidence on risks and risk outcome associations. With each annual GBD study, we update the GBD CRA to incorporate improved methods, new risks and risk outcome pairs, and new data on risk exposure levels and risk outcome associations. Methods We used the CRA framework developed for previous iterations of GBD to estimate levels and trends in exposure, attributable deaths, and attributable disability-adjusted life-years (DALYs), by age group, sex, year, and location for 84 behavioural, environmental and occupational, and metabolic risks or groups of risks from 1990 to 2017. This study included 476 risk outcome pairs that met the GBD study criteria for convincing or probable evidence of causation. We extracted relative risk and exposure estimates from 46 749 randomised controlled trials, cohort studies, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. Using the counterfactual scenario of theoretical minimum risk exposure level (TMREL), we estimated the portion of deaths and DALYs that could be attributed to a given risk. We explored the relationship between development and risk exposure by modelling the relationship between the Socio-demographic Index (SDI) and risk-weighted exposure prevalence and estimated expected levels of exposure and risk-attributable burden by SDI. Finally, we explored temporal changes in risk-attributable DALYs by decomposing those changes into six main component drivers of change as follows: (1) population growth; (2) changes in population age structures; (3) changes in exposure to environmental and occupational risks; (4) changes in exposure to behavioural risks; (5) changes in exposure to metabolic risks; and (6) changes due to all other factors, approximated as the risk-deleted death and DALY rates, where the risk-deleted rate is the rate that would be observed had we reduced the exposure levels to the TMREL for all risk factors included in GBD 2017. Findings In 2017,34.1 million (95% uncertainty interval [UI] 33.3-35.0) deaths and 121 billion (144-1.28) DALYs were attributable to GBD risk factors. Globally, 61.0% (59.6-62.4) of deaths and 48.3% (46.3-50.2) of DALYs were attributed to the GBD 2017 risk factors. When ranked by risk-attributable DALYs, high systolic blood pressure (SBP) was the leading risk factor, accounting for 10.4 million (9.39-11.5) deaths and 218 million (198-237) DALYs, followed by smoking (7.10 million [6.83-7.37] deaths and 182 million [173-193] DALYs), high fasting plasma glucose (6.53 million [5.23-8.23] deaths and 171 million [144-201] DALYs), high body-mass index (BMI; 4.72 million [2.99-6.70] deaths and 148 million [98.6-202] DALYs), and short gestation for birthweight (1.43 million [1.36-1.51] deaths and 139 million [131-147] DALYs). In total, risk-attributable DALYs declined by 4.9% (3.3-6.5) between 2007 and 2017. In the absence of demographic changes (ie, population growth and ageing), changes in risk exposure and risk-deleted DALYs would have led to a 23.5% decline in DALYs during that period. Conversely, in the absence of changes in risk exposure and risk-deleted DALYs, demographic changes would have led to an 18.6% increase in DALYs during that period. The ratios of observed risk exposure levels to exposure levels expected based on SDI (O/E ratios) increased globally for unsafe drinking water and household air pollution between 1990 and 2017. This result suggests that development is occurring more rapidly than are changes in the underlying risk structure in a population. Conversely, nearly universal declines in O/E ratios for smoking and alcohol use indicate that, for a given SDI, exposure to these risks is declining. In 2017, the leading Level 4 risk factor for age-standardised DALY rates was high SBP in four super-regions: central Europe, eastern Europe, and central Asia; north Africa and Middle East; south Asia; and southeast Asia, east Asia, and Oceania. The leading risk factor in the high-income super-region was smoking, in Latin America and Caribbean was high BMI, and in sub-Saharan Africa was unsafe sex. O/E ratios for unsafe sex in sub-Saharan Africa were notably high, and those for alcohol use in north Africa and the Middle East were notably low. Interpretation By quantifying levels and trends in exposures to risk factors and the resulting disease burden, this assessment offers insight into where past policy and programme efforts might have been successful and highlights current priorities for public health action. Decreases in behavioural, environmental, and occupational risks have largely offset the effects of population growth and ageing, in relation to trends in absolute burden. Conversely, the combination of increasing metabolic risks and population ageing will probably continue to drive the increasing trends in non-communicable diseases at the global level, which presents both a public health challenge and opportunity. We see considerable spatiotemporal heterogeneity in levels of risk exposure and risk-attributable burden. Although levels of development underlie some of this heterogeneity, O/E ratios show risks for which countries are overperforming or underperforming relative to their level of development. As such, these ratios provide a benchmarking tool to help to focus local decision making. Our findings reinforce the importance of both risk exposure monitoring and epidemiological research to assess causal connections between risks and health outcomes, and they highlight the usefulness of the GBD study in synthesising data to draw comprehensive and robust conclusions that help to inform good policy and strategic health planning. Copyright (C) 2018 The Author(s). Published by Elsevier Ltd

Study of the breakfast habits and its relationship with some factors in Semnan (Iran) pupils

Introduction: Proper nutrition is one of the essential factors to well being for children andadolescents. Meanwhile, breakfast has a major role to supply their requirement nutrients and energy.There are some experimental evidences that suggest that omitting breakfast negatively affectscognitive functioning. This survey was performed to study of breakfast habits and its relationshipswith some factors in Semnan (Iran) pupils during 2006.Materials and Methods: In this descriptive analytical study, 1193 pupils in different educationalgrades were selected by the multistage cluster sampling. Data were collected by using a questionnaireand analyzed with Kruskal Wallis, Mann - Whitney and Spearman Coefficient Correlation tests usingSPSS software.Results: The mean and standard deviation of age was 12.4±3.3 years old. 50.7% of them were boysand 49.3% were girls. 53.4% of the pupils stated that they always eat breakfast and the rest of them, donot eat irregularly. 4.4% of the pupils said they never eat breakfast. In this study, there was significantrelationship between breakfast habits and age (P<.01), educational grade (P<.0001), sex (P<.0001),the time of getting up in the morning (P<.0001), sleeping time at night (P<.0001), the education ofpupil’s mother (P<.04) , the education of pupil’s father (P<.05), the birth rank (P<.05) and theintervention of pupils in the breakfast planning (P<.0001). According to pupils’ breakfast for threecontinuous days, the relative consumption of bread (2.26), tea (2.20) and cheese (1.66) was higherthan other foods, such as milk, walnut, honey, egg, fruit and fruit juice.Conclusion: These finding showed that pupils need to learn more about both irregular intake ofbreakfast and various intake of nutritious foods and this issue must be considered by differentauthorities

mathcalRLmathcal{R}L- valued ff-ring homomorphisms and lattice-valued maps

In this paper, for each {it lattice-valued map} $Arightarrow L$ with some properties, a ring representation $Arightarrow mathcal{R}L$ is constructed. This representation is denoted by $tau_c$ which is an $f$-ring homomorphism and a $mathbb Q$-linear map, where its index $c$, mentions to a lattice-valued map. We use the notation $delta_{pq}^{a}=(a -p)^{+}wedge (q-a)^{+}$, where $p, qin mathbb Q$ and $ain A$, that is nominated as {it interval projection}. To get a well-defined $f$-ring homomorphism $tau_c$, we need such concepts as {it bounded}, {it continuous}, and $mathbb Q$-{it compatible} for $c$, which are defined and some related results are investigated. On the contrary, we present a cozero lattice-valued map $c_{phi}:Arightarrow L$ for each $f$-ring homomorphism $phi: Arightarrow mathcal{R}L$. It is proved that $c_{tau_c}=c^r$ and $tau_{c_{phi}}=phi$, which they make a kind of correspondence relation between ring representations $Arightarrow mathcal{R}L$ and the lattice-valued maps $Arightarrow L$, Where the mapping $c^r:Arightarrow L$ is called a {it realization} of $c$. It is shown that $tau_{c^r}=tau_c$ and $c^{rr}=c^r$.   Finally, we describe how $tau_c$ can be a fundamental tool to extend pointfree version of Gelfand duality constructed by B. Banaschewski

Comparing the Immunoregulatory Effects of Stem Cells from Human Exfoliated Deciduous Teeth and Bone Marrow-derived Mesenchymal Stem Cells

Stem cells from human exfoliated deciduous teeth (SHED) have been introduced recently and  possess characteristics similar to  mesenchymal stem  cells (MSCs). Because of  their convenient accessibility and safety of harvest, SHED can be a preferable source for the ever- increasing MSCs’ applications. While they are new, their immunoproperties have not been adequately studied. In this study, we aimed to explore the effect of SHED on T lymphocytes and compare it to conventional MSCs (BMMSCs). At first the isolated T lymphocytes were activated specifically/nonspecifically in vitro and cocultured  with  SHED   or  BMMSCs under  the  same  conditions,  subsequently  their proliferation and cytokine secretion (IL-2 and IFN-γ) were measured. In   our   experiment,  BMMSCs  and  SHED   inhibit  the  proliferation  and  cytokine production  of both  PHA  and alloantigen stimulated T lymphocytes in a dose-dependent manner. In direct and indirect contact to T lymphocytes, the inhibition of BMMSCs (but not of SHED)  was significantly different The cytokine production  from activated T cells was affected differently by two types of MSCs. The inhibition decreased by the separation of lymphocytes and MSCs by a semipermeable membrane, but it was not abolished. This study showed that SHED suppress the activation of human T lymphocytes in vitro like other  MSCs. Compared  to  BMMSCs, this suppression  was alleviated. In  the  equal conditions,  the  pattern  of  immune-modulation  of  BMMSCs and  SHED  was different, suggesting that SHED do not exert the exact mechanisms of BMMSCs' immunosuppression. This finding should be verified by further studies focused on the detailed mechanisms of the immunomodulation of SHED and also BMMSCs