The beginning of life is an intense experience for both mother and baby and sets the foundation for future interactions. Researchers have theorized that maternal infant bonding begins prenatally and continues on through the postnatal period. Mṻller (1996) examined that process to determine if prenatal bonding was related to postnatal bonding and discovered that there was only a modest correlation between the two. This led to speculation as to what variables, besides prenatal bonding, could influence postnatal bonding. Klaus & Kennell (1976) noted the detrimental effects of a lack of bonding in terms of abuse and attachment disorders and emphasized the urgency of understanding the process. Thus, an examination of factors that influence the initial attachment after birth is important in order to facilitate the experience for optimal outcomes. The purpose of this study was threefold: 1. Examine the relationship between a woman’s perceived birth experience and maternal infant bonding; 2. Examine the relationship between spirituality and maternal infant bonding; 3. Examine the relationship between perceived birth experience and maternal infant bonding. Women were recruited for an internet survey through various childbirth websites, nurses’ associations, and perinatal listserv communications. A total of 402 women responded to the survey, which consisted of 67 items in three instruments: Perception of Birth Scale; Spirituality; and Maternal Attachment Inventory. Of these respondents approximately 300 finished the survey completely and were used in the analyses. Slightly more than 190 left extensive comments regarding their experiences. Predictive Analytical Software (PASW 18) was used to analyze data and correlations were run on the measurements of the three instruments as well as a regression analysis. Perceived birth experience had the strongest correlation to maternal infant bonding and was found to have a stronger influence on bonding as well.

Background: Alzheimer’s disease (AD) is the most common form of dementia and is characterized by a progressive loss of memory, judgment, and thinking in older adults. The current treatment is cholinesterase inhibitors, which increase acetylcholine at the synapse. Medications with anticholinergic (AC) activity are given for a variety reasons including for the treatment of comorbid conditions or side effects of cholinesterase inhibitors (ChEIs). These drugs inhibit acetylcholine in the brain. Studies have shown the detrimental outcomes of using AC medications with ChEIs in older adults. Moreover, older patients take more medications and have an increased risk of developing AC toxicity as these effects are additive. The association between AC burden with functional, cognitive, and behavioral outcomes bears further evaluation. Methods: This study is a retrospective observational study that investigated the effect of AC medications on function, cognition, and behavior. Data was collected from charts on dementia patients who resided at Piedmont Geriatric Hospital. Descriptive statistics and GEE regression were performed using MS Excel 2007 and SPSS 18.0. Results: There were a total of 83 subjects included in this study with a median age of 77 years old and with a median length of stay of 536 days. 33.7% of the patients were taking cognitive-enhancing medications. The analysis found that AC burden was not a significant predictor of functional, cognitive or behavioral decline. Conclusion: The minimal amount of literature on this association, suggests that AC burden may have negative consequences on function, cognition and behavior in dementia patients. The study results provided inconclusive evidence about the association of AC burden on poorer functional, cognitive and behavioral outcomes. Future research in this field is needed to determine if there is a true association between worsening outcomes and AC burden.

HIV-infected individuals who abuse opiates have been found to have a higher incidence and a faster progression of HIV encephalitis. Astrocytes, the major support cells in the CNS, are known to play a critical role in the HIV neuropathy. Although astrocytes tend not to be productively infected by the HIV-1 virus, dysregulation of their pro- and anti- inflammatory cytokines/chemokines secretion is usually neurotoxic. Glutamate transport in astrocytes is reported to be impaired as well, which result in extrasynaptic excitatory neurotransmitter accumulation and over stimulation of postsynaptic neurons. It is long known that astrocytes from different brain regions have diverse responses to extracellular stimulants. However, few publications discuss the regional heterogeneity of astrocytes in HIV infected central nervous system. Based on the above information, we hypothesize that astroglia from different brain regions vary in their responses to HIV proteins and the responses could be influenced by co-treatment of morphine. To test this we cultured astrocytes from cerebral cortex, cerebellum and spinal cord, treated them with HIV-1 proteins Tat and gp120 with or without morphine and opioid receptor (mu, delta and kappa receptor) antagonist, naloxone. After 12-18 hours, conditioned medium from each group was analyzed using a Bio-Plex array. Cells from striatal cultures were harvested and lysed; proteins were extracted and evaluated with Western blotting to see whether EAAT2 expression on astrocytes is changed. Results showed that there were significant regional differences among three brain regions in cytokine/chemokine release, both in their basal secretion and in response to viral proteins. Astrocytes from spinal cord and cerebellum had a significantly higher basal secretion than those from cortical glia. All regions had increased cytokine/chemokine secretion when treated with Tat. Astroglia from the cortex showed the highest overall accumulation of cytokines/chemokines. Astroglia from the spinal cord had a slightly lower response overall, although KC expression was highest than other two groups in response to HIV-1 proteins. Astroglia from the cerebellum had a noticeably low response to Tat compared with those from spinal cord and cortex. However, concurrent morphine administration did not have a synergistic effect. No significant change in cytokines/chemokines release was seen when treated by gp120 with or without morphine. No significant change was found in EAAT2 expression on astrocytes either. In conclusion, astrocytes from different brain regions had different baseline secretion pattern and responses to viral protein. Tat had a noticeable effect in inducing cytokines/chemokines production in astrocytes from all brain regions, while limited change could be found with gp120 and morphine treatments. No significant change was found in EAAT2 expression on astrocytes.

Proteolytic processing of transmembrane receptors and ligands can have dramatic effects on cell signaling and subsequent cellular responses. Previous studies demonstrated that a disintegrin and metalloproteinase 10 (ADAM10) may cleave numerous B cell-expressed receptors, including the low affinity IgE receptor (CD23). However, lethality of ADAM10-deficient embryos has limited examination of these cleavage events in lymphocytes. To investigate their role in B cell development and function, we generated B cell-specific ADAM10 knockout mice. Intriguingly, deletion prevented development of the entire marginal zone B cell (MZB) lineage. Further analysis revealed that ADAM10 is required for S2 cleavage of the Notch2 receptor and initiation of Notch2 signaling, which is required for MZB development. Additionally, cleavage of CD23 was dramatically impaired in ADAM10-deficient B cells. This finding and results of ex vivo cleavage assays demonstrated that ADAM10 is the principal in vivo sheddase of CD23. Previous studies have demonstrated that Notch signaling and CD23 cleavage regulate antibody production. Accordingly, deletion of ADAM10 profoundly inhibited germinal center formation, and T-dependent and T-independent antibody responses to immunization, implicating ADAM10 as a novel regulator of adaptive immunity. Additionally, to determine the role of ADAM10 activity in hematopoiesis, we generated transgenic mice (A10Tg) that overexpress the protease on lymphoid and myeloid progenitors. Surprisingly, this markedly suppressed B2 cell development and promoted dramatic expansion of myeloid-derived suppressor cells (MDSCs) via a cell intrinsic mechanism. A10Tg MDSCs inhibited T cell proliferation and adoptive immunotherapy of B16 melanoma, resulting in exacerbated metastatic progression that was prevented by MDSC depletion. Thus, A10Tg mice represent a novel model for the examination of MDSC development and MDSC-mediated immune suppression in a tumor-free environment. Finally, hematopoietic stem cell cultures revealed that ADAM10 overexpression directs myeloid development by dysregulating Notch signaling via uncoupling the highly regulated proteolysis of Notch receptors. Collectively, these findings demonstrate that ADAM10 is a critical regulator of Notch signaling, B cell development, and MDSC expansion. Moreover, they have important implications for the treatment of numerous CD23 and Notch mediated pathologies, ranging from allergy to cancer.

The gram-positive bacterium Streptococcus sanguinis is a member of human indigenous oral microbialflora and has long been recognized as a key player in the bacterial colonization of the mouth. S. sanguinis is also the most common viridians streptococcal species implicated in infective endocarditis. Although many studies have focused on two-component systems in closely related Streptococcus species such as S. mutans, S. pneumoniae and S. gordonii; the mechanism of the response regulator in S. sanguinis is still unknown. The ability of S. sanguinis to adapt and thrive in hostile environments suggests this bacterium is capable of sensing and responding to various environmental stimuli. The present study clearly demonstrates that a number of RR genes, SSA_0204, SSA_0217, SSA_1810, SSA_1794, and SSA_1842, in S. sanguinis are essential to the recognition and response to various environmental stresses. Results from this study also identified genes SSA_0260, SSA_0261, and SSA-0262, involved in acidic tolerance and suppressed by SSA_0204 response regulator.

Hepatitis B virus is a member of the hepadnavirus family. The hepatitis B virus core gene codes for two proteins viz. core protein and pre-core protein. These proteins assemble to form particles viz. HBcAg and HBeAg respectively. The structure of the HBcAg has been widely studied but very little is known about the structure of HBeAg. Therefore, the aim of this study was to identify the disulfide bonding patterns in HBeAg. Recombinant HBeAg was isolated from E.coli and used for this study along with various mutants of HBeAg. There are four cysteines present in HBeAg each at position -7, 48, 61 and 107. From this study it can be inferred that the cysteine at 61 and 48 were found to be involved in inter-molecular disulfide bonds between the cysteine at 61 and 48 of other identical monomers. These di-mers were further inter-molecularly linked with cysteine at -7 to form chains. Moreover, the cysteine at -7 and cysteine at 107 were sometimes involved in intra-molecular disulfide bond formation. Thus, the HBeAg in a solution was found be particulate with a heterogeneous pattern of inter chain disulfide bonds.

Streptococci resident in the oral cavity have been linked to infective endocarditis (IE). While viridans streptococci are commonly studied and associated with IE, less research has been focused on Streptococcus pneumoniae. Two-component systems (TCSs), consisting of a histidine kinase (HK) protein and response regulator (RR) protein, are bacterial signaling systems that may mediate S. pneumoniae TIGR4 strain virulence in IE. To test this hypothesis, TCS RR mutants of TIGR4 were examined in vivo through use of rabbit models. There were 14 RR proteins identified and 13 RR mutants synthesized because SP_1227 was found to be essential. The requirement of the 13 RRs for S. pneumoniae growth in IE models was assessed by quantifying mutants after overnight inoculation in IE infected rabbits through use of real time PCR (qPCR), colony enumeration on antibiotic selection plates, and competitive index assays. Real time PCR pinpointed several candidate virulence factors. Candidate RR SP_0798 was selected to be further examined. In the in vivo model, mutant SP_0798 grew significantly less than our control mutant SP_1678, which encodes a hypothetical protein and grew at a comparable rate to wild-type TIGR4 strains. Literature and databases identified SP_0798 as the ciaR gene, which has roles in regulating many diverse cellular functions. Our data suggests that RR SP_0798 is a virulence factor of S. pneumoniae TIGR4 strain in IE. This research may place more emphasis on virulence factors and lead to novel methods to combat pneumococcal endocarditis.

The study objective was to determine cementum-dentin wall thickness along the furcation groove in maxillary bifurcated first premolars after preparation with three successively larger, 0.04 tapered, nickel titanium rotary files. Pre-instrumentation and post-instrumentation imaging was accomplished utilizing Cone Beam Computed Tomography. All data was analyzed using an ANOVA. Instrumentation resulted in a significant reduction in dentin-cementum wall thickness (p < .001). At mid-groove, predicted dentin-cementum wall thickness (95% CI) was equal to or less than the proposed standard (0.50 mm) for apical file sizes 30, 35, and 40 respectively. Instrumentation of the mid-groove in maxillary first premolars reduces dentin-cementum wall thickness to levels that may be insufficient to ensure tooth integrity.

The purpose of this study was to determine the number of rotations to fracture (cyclic fatigue) of the Profile® Vortex™ files (Dentsply Tulsa Dental Specialties, Tulsa, OK) compared to the EndoSequence™ files (Brasseler USA, Savannah, GA) using an in-vitro apparatus simulating a curved canal. Two hundred Profile® Vortex™ files of 25mm length were divided equally into ten groups, one for each of the Profile® Vortex™ files 20/0.04, 20/0.06, 25/0.04, 25/0.06, 30/0.04, 30/0.06, 35/0.04, 35/0.06, 40/0.04, and 40/0.06. Two hundred EndoSequence™ files of 25mm length were divided equally into ten groups of the same tip and taper sizes analogous to the Profile® Vortex™ file groups. Files were rotated at 500 rpm in a fixed groove in the metal block of the apparatus. The angle of deflection for all files was fixed at 33 degrees, determined using the Schneider method. The time from initiation of rotation to fracture was recorded and rotations to fracture were calculated. The data collected was analyzed using a multi-way ANOVA, followed by specific post-hoc contrasts comparing the two brands for each tip and taper combination. The results demonstrated that the Profile® Vortex™ files required significantly greater rotations to fracture than the EndoSequence™ (p < 0.001) in all tip sizes in both 0.04 and 0.06 tapers. Profile® Vortex™ files exhibited a greater resistance to cyclic fatigue than the EndoSequence™ files.

Purpose: To assess the effect of dental Medicaid reforms in the state of Virginia on dental plan performance. Methods: This project is a retrospective cohort study of 825,000 dental claims obtained from the Virginia Department of Medical Assistance Services. This cohort includes dental claims for children enrolled in Virginia’s Medicaid program from July 1, 2002 through June 30, 2008. The independent variable was enrollment pre or post policy reform with July 1, 2005 as the period dividing date. The dependent variable was dental benefit utilization measured as the average number of restorative, preventative, and total procedures. Statistical methods include Welch’s t-test and repeated measures mixed model ANOVA controlling for gender, race, age, length of enrollment, gaps in patient enrollment, citizenship status, and geographic location. Results: This cohort of data showed a significant increase in the total number of procedures utilized by enrolled children (P value < 0.001). There were also significant increases in restorative services across all periods of enrollment. Conclusion: The consolidation of Virginia’s multiple managed care programs into a single vendor with increased reimbursement levels resulted in increased in access to care and improved utilization of dental services for children enrolled in Medicaid.