No association between islet cell antibodies and coxsackie B, mumps, rubella and cytomegalovirus antibodies in non-diabetic individuals aged 7–19 years

Viral antibodies were tested in a cohort of 44 isletcell antibody-positive individuals age 7–19 years, and 44 of their islet cell antibody-negative age and sex-matched classmates selected from a population study of 4208 pupils who had been screened for islet cell antibodies. Anti-coxsackie B1-5 IgM responses were detected in 14 of 44 (32%) of the islet cell antibody-positive subjects and in 7 of 44 (16%) control subjects. This difference did not reach the level of statistical significance. None of the islet cell antibody-positive subjects had specific IgM antibodies to mumps, rubella, or cytomegalovirus. There was also no increase in the prevalence or the mean titres of anti-mumps-IgG or IgA and anti-cytomegalovirus-IgG in islet cell antibody-positive subjects compared to control subjects. These results do not suggest any association between islet cell antibodies, and possibly insulitis, with recent mumps, rubella or cytomegalo virus infection. Further studies are required to clarify the relationship between islet cell antibodies and coxsackie B virus infections

Core business prospects and the management of internal corporate ventures

Abstract: Corporations with attractive core business prospects focus their attention on those core businesses and away from ICVs they may be pursuing, thus influencing how those ICVs are treated from a corporate parenting perspective and, in turn, how well they perform. Using data collected from 145 ICVs operating in 72 corporate parents, this research reveals that corporations with more attractive core businesses grant greater planning autonomy to their ICVs’ managers, and planning autonomy contributes to ICV performance. Additional results reveal the moderating effects within our structural model of venture manager experience and the similarity of the ICV’s product to those of other businesses within the corporation. Considered collectively, this research demonstrates why corporations that “need” their ICVs to be successful – because of poor prospects in their core businesses – are most likely to mismanage them. Unattractive core business prospects can be viewed as justifying corporate managers’ involvement in the direct management of their firms’ ICVs. However, venture planning autonomy is needed to avoid placing undue expectations on ICVs as the “saviors” of corporate performance. By extension, this need for autonomy is also anticipated to apply to other entrepreneurial contexts where experimentation and learning are significant concerns (e.g., business incubators, corporate venture capital investments, new venture divisions). Plain English Summary: This research demonstrates how and why corporations that have attractive core business operations are most likely to be good corporate parents to their internal corporate ventures (ICVs), and vice versa. In a sense, when it comes to internal corporate venturing, “the rich corporations get richer, and the poor corporations get poorer.” Parent corporations with more attractive core business prospects were found to grant greater planning autonomy to the managers of their ICVs, and autonomy is needed to give ICV managers the discretion and flexibility they need when navigating their ventures though unchartered business territory. Overall, this research demonstrates the importance of corporate managers (1) granting ICV managers autonomy in planning their venture operations, (2) being willing to consider engaging in internal corporate venturing even though their firms’ existing, core business operations may be attractive (i.e., before these ICVs “need” to be successful), and (3) not putting too much pressure on ICVs to “perform,” and avoiding meddling in the management of those ventures, when prospects in the corporation’s core business are unattractive. We argue that autonomy is likely efficacious in most entrepreneurial contexts where experimentation and learning are significant concerns (e.g., business incubators, corporate venture capital investments, new venture divisions)

Plant and soil's \u3b415N are regulated by climate, soil nutrients, and species diversity in alpine grasslands on the northern Tibetan Plateau

Nitrogen (N) cycling is a critical pathway by which producer, consumer, and decomposer interact with each other and with environmental circumstances simultaneously. The natural abundance composition of 15N/14N in plants and soils (termed as \u3b415Nplant and \u3b415Nsoil), as well as the difference between them (\u3b415Nsoil-to-plant = \u3b415Nplant 12\u3b415Nsoil), is a useful tool for better understanding ecosystem N cycling. However, the drivers and mechanisms of ecosystem N cycling in alpine grasslands on the Tibetan Plateau are mostly unknown, especially across different grassland types at a regional scale. To fill this knowledge gap, we measured \u3b415Nplant (200 samples of top-dominant species) and \u3b415Nsoil (85 samples of top-layer soils, 0\u201320 cm) at nine sites that represent zonal communities of alpine deserts, steppes, and meadows in North Tibet, and calculated the corresponding \u3b415Nsoil-to-plant. Our results showed that \u3b415Nplant, \u3b415Nsoil, and \u3b415Nsoil-to-plant were significantly different among the three zonal grassland types (analysis of differences with non-parametric Kruskal Test, P < 0.05), with the lowest values in meadows and the highest values in deserts. Regression analyses showed that the \u3b415Nplant, \u3b415Nsoil, and \u3b415Nsoil-to-plant decreased with the increases of growing season precipitation (GSP) and habitat aridity index (Aridity), soil organic carbon (SOC) and soil total nitrogen (STN), plant species richness, Shannon diversity index, and plant community productivity, whereas increased with the increases of accumulated active temperature (AccT) and soil total phosphorus (STP) across alpine grassland types at the regional scale. Multiple linear models with analysis of covariance (ANCOVA) confirmed GSP to be the most critical driver, which alone explained most variances of \u3b415Nplant (56%), \u3b415Nsoil (62%), and \u3b415Nsoil-to-plant (35%). However, structural equation modeling performed better than multiple linear modeling in predicting \u3b415Nplant (76% vs. 66%) and worse in predicting \u3b415Nsoil (79% vs. 84%) and \u3b415Nsoil-to-plant (31% vs. 46%), likely due to the exclusion of collinear predictors and the removal of non-significant influencing paths. Overall, this study has highlighted the importance to uncover the complexity of climate, soil nutrients, and vegetation properties in networking to drive the different components of ecosystem N cycling in alpine grasslands on the Tibetan Plateau

Differential effects of the neuroprotectant lubeluzole on bovine and mouse chromaffin cell calcium channel subtypes

1. The effects of lubeluzole (a neuroprotective benzothiazole derivative) and its (−) enantiomer R91154 on whole-cell currents through Ca(2+) channels, with 10 mM Ba(2+) as charge carrier (I(Ba)), have been studied in bovine and mouse voltage-clamped adrenal chromaffin cells. Currents generated by applying 50 ms depolarizing test pulses to 0 mV, from a holding potential of −80 mV, at 10 s intervals had an average magnitude of 1 nA. 2. Lubeluzole and R91154 blocked the peak I(Ba) of bovine chromaffin cells in a time and concentration-dependent manner; their IC(50)s were 1.94 μM for lubeluzole and 2.54 μM for R91154. In a current-voltage protocol, lubeluzole (3 μM) inhibited peak I(Ba) at all test potentials. However, no obvious shifts of the I-V curve were detected. 3. After 10 min exposure to 3 μM lubeluzole, the late current (measured at the end of the pulse) was inhibited more than the peak current. Upon wash out of the drug, the inactivation reversed first and then the peak current recovered. 4. Blockade of peak current was greater at more depolarizing holding potentials (i.e. 35% at −110 mV and 87% at −50 mV, after 10 min superfusion with lubeluzole). Inactivation of the current was pronounced at −110 mV, decreased at −80 mV and did not occur at −50 mV. 5. Intracellular dialysis of bovine voltage-clamped chromaffin cells with 3 μM lubeluzole caused neither blockade nor inactivation of I(Ba). The external application of 3 μM lubeluzole to those dialysed cells produced inhibition as well as inactivation of I(Ba). 6. The effects of lubeluzole (3 μM) on I(Ba) in mouse chromaffin cells were similar to those in bovine chromaffin cells. At −80 mV holding potential, a pronounced inactivation of the current led to greater blockade of the late I(Ba) (66%) as compared with peak I(Ba) (46% after 10 min superfusion with lubeluzole). 7. In mouse chromaffin cells approximately half of the whole-cell I(Ba) was sensitive to 3 μM nifedipine (L-type Ca(2+) channels) and the other half to 3 μM ω-conotoxin MVIIC (non-L-type Ca(2+) channels). In ω-conotoxin MVIIC-treated cells, 3 μM lubeluzole caused little blockade and inactivation of I(Ba). However in nifedipine-treated cells, lubeluzole caused a pronounced blockade and inactivation of I(Ba) that reversed upon wash out of the compound. 8. The results are compatible with the idea that lubeluzole preferentially blocks non-L-types of voltage-dependent Ca(2+) channels expressed by bovine and mouse chromaffin cells. The higher concentrations of the compound also block L-type Ca(2+) channels. The mechanism of inhibition involves the access of lubeluzole to the open channel from the outside of the cell and promotion of its inactivation. The differential blockade of Ca(2+) channel subtypes might contribute to the neuroprotective actions of lubeluzole (which exhibit stereoselectivity). However, in view of the lack of stereoselectivity in blocking Ca(2+) channels, this effect cannot be the only explanation for the protective activity of lubeluzole in stroke

Assessing the effect of multibracket appliance treatment on tooth color by using electronic measurement

Abstract Background The purpose of this study was to investigate how tooth color is affected by multibracket appliance (MBA) treatment. Methods The color of teeth #14 to #24 of 15 patients with MBA was measured on body and gingival tooth segments using the spectrophotometer Shade Inspector™. Colors of both segments were recorded before start of MBA treatment (baseline T0), end of MBA treatment (T1; 2 years ±0.3), and 3 months after T1 (T2). A 2D color system and a 3D system served as reference systems. Multilevel models were used to analyze color change within segments and to compare the difference in color change between segments (treatment effect). Results 2D system. Changes within tooth segments from T0 to T2 were at worst 2.0 units (ΔE in the gingival segment), which is less than the threshold of 2.7 units for a clinically meaningful difference. Confidence intervals for the treatment effect indicated no clinically important differences in color change between body and gingival segments. 3D system. Changes within tooth segments from T0 to T2 were at worst 2.3 units (ΔE in the body segment), which is less than the threshold of 2.7 units for a clinically meaningful difference. Confidence intervals for the treatment effect indicated no clinically important differences in color change between body and gingival segments. Thus, MBA treatment did not lead to clinically relevant changes in tooth color. Conclusion Within the limitation of this study the MBA treatment can be seen as a safe method with respect to tooth color

Effects of Dehydroepiandrosterone Sulfate on the Evoked Cortical Activity of Controls and of Brain-Injured Rats

Dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) are sex hormone precursors which exert marked neurotrophic and/or neuroprotective activity in the central nervous system (CNS). In the present electrophysiological experiments, we studied the effects of peripherally administered DHEAS on responses of the primary somatosensory (SSI) and motor cortices (MI) of (i) anesthetized controls and (ii) MI focal cold-lesioned rats. (iii) The effects of DHEAS on the field excitatory postsynaptic potentials (fEPSPs) were also studied in vitro brain slices. DHEAS (50 mg/kg) was injected subcutaneously 12 h before and immediately after cold lesion induction. The anesthetized rats were fixed in a stereotaxic frame, the SSI and MI were exposed, and control SSI and MI responses were evoked by contralateral whisker pad stimulation. After registration of the evoked responses for a 35-min period, a copper cylinder (2 mm in diameter) cooled with a mixture of acetone and dry ice (-78 degrees C) was applied to produce a lesion in the MI and the registration of the evoked responses was then continued for an additional 360 min. In the controls, DHEAS administration resulted in slight increases in amplitude of both the SSI and the MI responses. After focal cold lesion induction, the most significant reduction in amplitude was observed at the focus of the lesion in the primary MI, but the amplitudes of the SSI responses were also decreased. After 3-5 h of lesion induction, the amplitudes started to increase around the injury in the primary MI, while the SSI response had already started to recover 2 h after induction of the MI lesion. In the course of the postlesion recovery period, the MI responses peripherally to the center of the lesion frequently exhibited extremely high and low amplitudes. The paired-pulse paradigm revealed changing, but basically high levels of disinhibition and facilitation in extended cortical areas after focal cortical cold lesion induction. The deviations (e.g., the extremely augmented responses) in cortical functioning of the anesthetized rats were unambiguously diminished by DHEAS administration, and the period required for the cortical responses to recover was significantly shorter after the steroid treatment. In the in vitro studies, however, DHEAS administration resulted in an enhanced level of disinhibition in extended cortical areas of both the hemispheres. This observation draws attention to the possible differences between the results obtained in different models (in vitro vs. in situ). Nevertheless, all the presented data suggest that DHEAS treatment might have neuroprotective effect on the neocortex at least at a short-time scale