Comparison of Salivary Glucose and Serum Glucose Concentration in Non-Insulin Dependent Diabetes Mellitus Patients: A Case Control Study

The present study titled “Comparison of Salivary Glucose and Serum Glucose concentration in Non-Insulin dependent Diabetes Mellitus patients” was conducted between March 2010 and April 2011 in the Out Patient Department of Voluntary Health Services, Adyar, Chennai to estimate the Salivary Glucose and Serum Glucose concentration in Non-Insulin dependent Diabetes Mellitus patients, to estimate the Salivary Glucose and Serum Glucose concentration in Healthy control group and finally to correlate these Salivary Glucose and Serum Glucose concentrations in Non-Insulin Dependent Diabetes Mellitus patients and healthy controls. The study group comprised of a total number of 80 patients. Out of the 80 patients, 40 were Healthy controls and the other 40 were suffering from Type 2 Diabetes Mellitus. Informed consent was taken from all subjects before including them in the study. Participants with infectious diseases during one month before saliva sampling, active dental abcesses, and collagen vascular diseases were excluded from the study. The experimental subjects were made to sit comfortably on a chair. Relevant demographic data was collected. An Intra Oral examination was carried out. Whole un-stimulated saliva was collected as well as the blood sample was collected. Saliva and blood samples were collected in sterile test tubes, immediately transferred aseptically to sterile tubes and frozen on dry ice and alcohol. The samples were stored in styroform boxes containing dry ice and carried to a freezer where they are left until time of assessment of the Salivary glucose and Serum glucose. The study documents the following data: 1. Among the 80 subjects 48 (60%) were females and 32 (40%) were males. 2. The minimum age among the subjects was 28yrs and maximum was 75yrs with a mean of 50.97 yrs. 3. Among the 40 subjects in the Control group there was 1 male and 3 females in the below 35yrs category, 5 males and 4 females in the 36-45yrs category, 5 males and 8 females in the 46-55yrs category and finally 5 males and 9 females in the above 55yrs category. 4. As this was an age and sex matched study, among 40 subjects in the Diabetic group there was 1 male and 3 females in the below 35yrs category, 5 males and 4 females in the 36-45yrs category, 5 males and 8 females in the 46-55yrs category and finally 5 males and 9 females in the above 55yrs category. 5. The distribution of Salivary glucose among the 40 subjects in the Healthy controls ranged from 0mg/dl to 8mg/dl. 6. Similarly, the Salivary glucose level distribution among the diabetics varied from 0mg/dl to 8mg/dl. 7. The Mean fasting blood glucose among the healthy controls was 101.63mg/dl for males and 93.54mg/dl for females. 8. The Mean fasting blood glucose among the diabetics was 208.13mg/dl for males and 197.67mg/dl for females. 9. A significant correlation was found between Age and Fasting blood glucose among the Healthy controls. 10. An insignificant correlation was found between the Salivary glucose and Fasting serum glucose level in the Healthy controls. 11. An insignificant correlation was found between the Salivary glucose and Fasting serum glucose levels in the Diabetic group. 12. Finally, an insignificant correlation was found between the Salivary glucose and Serum glucose. To conclude, Salivary glucose concentrations showed no difference between the Type 2 Diabetic and the Control group. This implies that the association of high Fasting serum glucose with high Salivary Glucose levels is an infrequent observation which may be affected by metabolic control of the disease. A large number of studies have been done in an attempt to check for the efficacy of Saliva as a diagnostic tool in Diabetes Mellitus. Unfortunately, there are no conclusive results. While the results of some studies give a go ahead to the usage of saliva as a diagnostic tool there are others which disapprove of it. The need of the hour is larger studies that need to be performed in various parts of the world among different populations with different dietary patterns before a conclusive result is achieved. Hence, the usage of salivary glucose as the only tool for evaluating glycemic status is debatable. Studies to compare long term indicators of glycemic status like HbA1C, fructosamine levels with salivary glucose / glycated proteins should be under-taken with a larger sample size as well as keeping the importance of regional variations in mind

Actinic cheilitis: A review

Actinic cheilitis (AC) is a chronic inflammatory disorder of the lips that is caused by prolonged exposure to sunlight in susceptible individuals. It affects the vermilion region of the lower lip almost exclusively. UV-B rays with a wavelength of 290-320 nm are held responsible for the sunlight-induced damage. The exact mechanism of the development of AC is unclear. It is considered to be potentially malignant

Microglia Impairs Proliferation and Induces Senescence In-Vitro in NGF Releasing Cells Used in Encapsulated Cell Biodelivery for Alzheimer’s Disease Therapy

There is no cure yet available for Alzheimer’s disease (AD). We recently optimized encapsulated cell biodelivery (ECB) devices releasing human mature nerve growth factor (hmNGF), termed ECB-NGF, to the basal forebrain of AD patients. The ECB-NGF delivery resulted in increased CSF cholinergic markers, improved glucose metabolism, and positive effects on cognition in AD patients. However, some ECB-NGF implants showed altered hmNGF release post-explantation. To optimize the ECB-NGF platform for future therapeutic purposes, we initiated in-vitro optimization studies by exposing ECB-NGF devices to physiological factors present within the AD brain. We report here that microglia cells can impair hmNGF release from ECB-NGF devices in-vitro, which can be reversed by transferring the devices to fresh culture medium. Further, we exposed the hmNGF secreting human ARPE-19 cell line (NGC0211) to microglia (HMC3) conditioned medium (MCM; untreated or treated with IL-1β/IFNγ/Aβ40/Aβ42), and evaluated biochemical stress markers (ROS, GSH, ΔΨm, and Alamar Blue assay), cell death indicators (Annexin-V/PI), cell proliferation (CFSE retention and Ki67) and senescence markers (SA-β-gal) in NGC0211 cells. MCMs from activated microglia reduced cell proliferation and induced cell senescence in NGC0211 cells, which otherwise resist biochemical alterations and cell death. These data indicate a critical but reversible impact of activated microglia on NGC0211 cells

Feasibility and therapeutical potential of local intracerebral encapsulated cell biodelivery of BDNF to App NL−G−F knock-in Alzheimer mice

Abstract Background Alzheimer’s disease (AD) is an age-related disease characterized by altered cognition, neuroinflammation, and neurodegeneration against which there is presently no effective cure. Brain-derived neurotrophic factor (BDNF) is a key neurotrophin involved in the learning and memory process, with a crucial role in synaptic plasticity and neuronal survival. Several findings support that a reduced BDNF expression in the human brain is associated with AD pathogenesis. BDNF has been proposed as a potential therapy for AD, but BDNF has low brain penetration. In this study, we used an innovative encapsulated cell biodelivery (ECB) device, containing genetically modified cells capable of releasing BDNF and characterized its feasibility and therapeutic effects in the novel App knock-in AD mouse model (App NL−G−F ). Methods ECB’s containing human ARPE-19 cells genetically modified to release BDNF (ECB-BDNF devices) were stereotactically implanted bilaterally into hippocampus of 3-month-old App NL−G−F mice. The stability of BDNF release and its effect on AD pathology were evaluated after 1, 2-, and 4-months post-implantation by immunohistochemical and biochemical analyses. Exploratory and memory performance using elevated plus maze (EPM) and Y-maze test were performed in the 4-months treatment group. Immunological reaction towards ECB-BDNF devices were studied under ex vivo and in vivo settings. Results The surgery and the ECB-BDNF implants were well tolerated without any signs of unwanted side effects or weight loss. ECB-BDNF devices did not induce host-mediated immune response under ex vivo set-up but showed reduced immune cell attachment when explanted 4-months post-implantation. Elevated BDNF staining around ECB-BDNF device proximity was detected after 1, 2, and 4 months treatment, but the retrieved devices showed variable BDNF release. A reduction of amyloid-β (Aβ) plaque deposition was observed around ECB-BDNF device proximity after 2-months of BDNF delivery. Conclusions The result of this study supports the use of ECB device as a promising drug-delivery approach to locally administer BBB-impermeable factors for treating neurodegenerative conditions like AD. Optimization of the mouse-sized devices to reduce variability of BDNF release is needed to employ the ECB platform in future pre-clinical research and therapy development studies

Positive and negative selection shape the human naive B cell repertoire

Although negative selection of developing B cells in the periphery is well described, yet poorly understood, evidence of naive B cell positive selection remains elusive. Using 2 humanized mouse models, we demonstrate that there was strong skewing of the expressed immunoglobulin repertoire upon transit into the peripheral naive B cell pool. This positive selection of expanded naive B cells in humanized mice resembled that observed in healthy human donors and was independent of autologous thymic tissue. In contrast, negative selection of autoreactive B cells required thymus-derived Tregs and MHC class II-restricted self-antigen presentation by B cells. Indeed, both defective MHC class II expression on B cells of patients with rare bare lymphocyte syndrome and prevention of self-antigen presentation via HLA-DM inhibition in humanized mice resulted in the production of autoreactive naive B cells. These latter observations suggest that Tregs repressed autoreactive naive B cells continuously produced by the bone marrow. Thus, a model emerged, in which both positive and negative selection shaped the human naive B cell repertoire and that each process was mediated by fundamentally different molecular and cellular mechanisms