Definition of anatomical zero positions for assessing shoulder pose with 3D motion capture during bilateral abduction of the arms

Background: Surgical interventions at the shoulder may alter function of the shoulder complex. Clinically, the outcome can be assessed by universal goniometry. Marker-based motion capture may not resemble these results due to differing angle definitions. Methods: The clinical inspection of bilateral arm abduction for assessing shoulder dysfunction is performed with a marker based 3D optical measurement method. An anatomical zero position of shoulder pose is proposed to determine absolute angles according to the Neutral-0-Method as used in orthopedic context. Static shoulder positions are documented simultaneously by 3D marker tracking and universal goniometry in 8 young and healthy volunteers. Repetitive bilateral arm abduction movements of at least 150° range of motion are monitored. Similarly a subject with gleno-humeral osteoarthritis is monitored for demonstrating the feasibility of the method and to illustrate possible shoulder dysfunction effects. Results: With mean differences of less than 2°, the proposed anatomical zero position results in good agreement between shoulder elevation/depression angles determined by 3D marker tracking and by universal goniometry in static positions. Lesser agreement is found for shoulder pro-/retraction with systematic deviations of up to 6°. In the bilateral arm abduction movements the volunteers perform a common and specific pattern in clavicula-thoracic and gleno-humeral motion with maximum shoulder angles of 32° elevation, 5° depression and 45° protraction, respectively, whereas retraction is hardly reached. Further, they all show relevant out of (frontal) plane motion with anteversion angles of 30° in overhead position (maximum abduction). With increasing arm anteversion the shoulder is increasingly retroverted, with a maximum of 20° retroversion. The subject with gleno-humeral osteoarthritis shows overall less shoulder abduction range of motion but with increased out-of-plane movement during abduction. Conclusions: The proposed anatomical zero definition for shoulder pose fills the missing link for determining absolute joint angles for shoulder elevation/depression and pro-/retraction. For elevation-/depression the accuracy suits clinical expectations very well with mean differences less than 2° and limits of agreement of 8.6° whereas for pro-/retraction the accuracy in individual cases may be inferior with limits of agreement of up to 24.6°. This has critically to be kept in mind when applying this concept to shoulder intervention studies

Foliar Magnesium supply increases the abundance of RuBisCO of Mg-deficient maize plants

Magnesium is a vital macronutrient for plants and is involved in a series of essential physiological processes, e.g., carbohydrate partitioning and photosynthesis. The latter is strictly Mg-dependent, as Mg is the central atom of chlorophyll, and is also required for the de novo synthesis of sugars; this pathway revolves around the activity of the enzyme RuBisCO. When plants are subject to Mg limiting conditions, development as well as yield is reduced. The foliar resupply of Mg, contrary to traditional resupply to the roots, has the advantage of delivering the element directly to the site of highest physiological demand. Thus, the aim of this research is to compare the effects of both resupply methods on the physiology and nutritional status of Mg-deficient plants to see whether foliar application compared to root fertilization can properly improve plant growth after Mg deficiency conditions.Maize plants were cultivated in hydroponics in order to set up a Mg deficient root environment. MgSO4 was then resupplied alternatively to the leaves or to the root. Under Mg-limiting conditions, RuBisCO abundance, as well as the total content of Mn, Zn, Fe, and Cu were severely reduced. This state was significantly ameliorated by the foliar resupply of MgSO4, although the highest increase in biomass production was observed in response to root resupply. The foliar resupply of MgSO4 upregulated the process of photosynthesis in Mg-deprived plants. In this context, the foliar MgSO4 application was able to return RuBisCO abundance to control levels in Mg-deficient plants

Decreased HIV diversity after allogeneic stem cell transplantation of an HIV-1 infected patient: a case report

The human immunodeficiency virus type 1 (HIV-1) coreceptor use and viral evolution were analyzed in blood samples from an HIV-1 infected patient undergoing allogeneic stem cell transplantation (SCT). Coreceptor use was predicted in silico from sequence data obtained from the third variable loop region of the viral envelope gene with two software tools. Viral diversity and evolution was evaluated on the same samples by Bayesian inference and maximum likelihood methods. In addition, phenotypic analysis was done by comparison of viral growth in peripheral blood mononuclear cells and in a CCR5 (R5)-deficient T-cell line which was controlled by a reporter assay confirming viral tropism. In silico coreceptor predictions did not match experimental determinations that showed a consistent R5 tropism. Anti-HIV directed antibodies could be detected before and after the SCT. These preexisting antibodies did not prevent viral rebound after the interruption of antiretroviral therapy during the SCT. Eventually, transplantation and readministration of anti-retroviral drugs lead to sustained increase in CD4 counts and decreased viral load to undetectable levels. Unexpectedly, viral diversity decreased after successful SCT. Our data evidence that only R5-tropic virus was found in the patient before and after transplantation. Therefore, blocking CCR5 receptor during stem cell transplantation might have had beneficial effects and this might apply to more patients undergoing allogeneic stem cell transplantation. Furthermore, we revealed a scenario of HIV-1 dynamic different from the commonly described ones. Analysis of viral evolution shows the decrease of viral diversity even during episodes with bursts in viral load

The regulation of SIRT2 function by cyclin-dependent kinases affects cell motility

Cyclin-dependent kinases (Cdks) fulfill key functions in many cellular processes, including cell cycle progression and cytoskeletal dynamics. A limited number of Cdk substrates have been identified with few demonstrated to be regulated by Cdk-dependent phosphorylation. We identify on protein expression arrays novel cyclin E–Cdk2 substrates, including SIRT2, a member of the Sirtuin family of NAD+-dependent deacetylases that targets α-tubulin. We define Ser-331 as the site phosphorylated by cyclin E–Cdk2, cyclin A–Cdk2, and p35–Cdk5 both in vitro and in cells. Importantly, phosphorylation at Ser-331 inhibits the catalytic activity of SIRT2. Gain- and loss-of-function studies demonstrate that SIRT2 interfered with cell adhesion and cell migration. In postmitotic hippocampal neurons, neurite outgrowth and growth cone collapse are inhibited by SIRT2. The effects provoked by SIRT2, but not those of a nonphosphorylatable mutant, are antagonized by Cdk-dependent phosphorylation. Collectively, our findings identify a posttranslational mechanism that controls SIRT2 function, and they provide evidence for a novel regulatory circuitry involving Cdks, SIRT2, and microtubules

Claudin-12 is not required for blood-brain barrier tight junction function

Background The blood-brain barrier (BBB) ensures central nervous system (CNS) homeostasis by strictly controlling the passage of molecules and solutes from the bloodstream into the CNS. Complex and continuous tight junctions (TJs) between brain endothelial cells block uncontrolled paracellular diffusion of molecules across the BBB, with claudin-5 being its dominant TJs protein. However, claudin-5 deficient mice still display ultrastructurally normal TJs, suggesting the contribution of other claudins or tight-junction associated proteins in establishing BBB junctional complexes. Expression of claudin-12 at the BBB has been reported, however the exact function and subcellular localization of this atypical claudin remains unknown. Methods We created claudin-12-lacZ-knock-in C57BL/6J mice to explore expression of claudin-12 and its role in establishing BBB TJs function during health and neuroinflammation. We furthermore performed a broad standardized phenotypic check-up of the mouse mutant. Results Making use of the lacZ reporter allele, we found claudin-12 to be broadly expressed in numerous organs. In the CNS, expression of claudin-12 was detected in many cell types with very low expression in brain endothelium. Claudin-12(lacZ/lacZ) C57BL/6J mice lacking claudin-12 expression displayed an intact BBB and did not show any signs of BBB dysfunction or aggravated neuroinflammation in an animal model for multiple sclerosis. Determining the precise localization of claudin-12 at the BBB was prohibited by the fact that available anti-claudin-12 antibodies showed comparable detection and staining patterns in tissues from wild-type and claudin-12(lacZ/lacZ) C57BL/6J mice. Conclusions Our present study thus shows that claudin-12 is not essential in establishing or maintaining BBB TJs integrity. Claudin-12 is rather expressed in cells that typically lack TJs suggesting that claudin-12 plays a role other than forming classical TJs. At the same time, in depth phenotypic screening of clinically relevant organ functions of claudin-12(lacZ/lacZ) C57BL/6J mice suggested the involvement of claudin-12 in some neurological but, more prominently, in cardiovascular functions