Tibiofemoral joint instability reduces patient satisfaction after total knee arthroplasty (TKA). However, surgeons sometimes encounter excessive medial joint laxity without medial over-release on the tibial side. It was hypothesized that over-resection of the posteromedial femoral condyle can injure the medial stabilizers, especially the posterior oblique ligament (POL) at its femoral attachments.
 
  Thirteen fixed cadaveric knees were exposed, and 3 anatomical points were identified the posterior edge and midpoint of the POL femoral attachment, and the posterior edge of the superficial medial collateral ligament (sMCL) femoral attachment. The distance from the surface of the posteromedial femoral condyle to each point was measured. Correlations between each point and the anterior-posterior or medial-lateral dimensions of the distal femur were also calculated.
 
  The average distances to the posterior edge and midpoint of the POL femoral attachment and the posterior edge of the sMCL femoral attachment were 13.7mm (9.0-18.4), 17.9mm (11.5-22.6), and 22.7mm (14.7-29.4), respectively. There were moderate correlations between the distance to each point and the anterior-posterior or medial-lateral dimensions of the distal femur.
 
  The minimal distance from the surface of the posteromedial condyle to the POL posterior edge was 9.0mm. Over-resection of the posteromedial femoral condyle, even with a general TKA femoral component, might injure the POL at its femoral attachments, especially in patients with small distal femurs, while the sMCL is rarely damaged.
 
  Level IV.
 Level IV.Many governments have seen digital health technologies as promising tools to tackle the current COVID-19 pandemic. A much-talked example in this context involves the recent deluge of digital contact tracing apps (DCT) aimed at detecting Covid-19 exposure. In this short contribution we look at the bio-political justification of this phenomenon and reflect on whether DCT apps constitute, as it is often argued, a serious potential breach of our right to privacy. Despite praising efforts attempting to develop legal and ethical frameworks for DCT apps' usage; we argue that such endeavours are not sufficient to tackle the more fundamental problem of mass surveillance, which will remain largely unaddressed unless we deal with the biopolitical arguments presented and resort to a technical and structural defence.
  Induced polyploidy serves as an efficient approach in extricating genetic potential of cells. During polyploidization, multiple sets of chromosomes are derived from the same organism resulting in the development of an autopolyploid. Alterations owing to artificially induced polyploidy level significantly influence internal homeostatic condition of resultant cells.
 
  Induced autopolyploidy transpires as a result of an increase in the size of genome without any change in elementary genetic material. Such autopolyploidy, artificially induced via application of antimitotic agents, brings about a lot of beneficial changes in plants, coupled with very few detrimental effects. Induced autopolyploids exhibit superior adaptability, endurance to biotic and abiotic stresses, longer reproductive period and enzyme diversity coupled with enhanced rate of photosynthesis and gene action in comparison to their diploid counterparts. However, reduced rate of transpiration and growth, delay in flowering are some of the demerittance.
  This study aimed to identify the incidence of ophthalmic complications of giant cell arteritis (GCA) among subjects with negative temporal artery biopsy (TAB) and to determine if duration of prednisone exposure relative to GCA diagnosis was associated with ophthalmic complications in TAB-negative subjects.
 
  The U.S. Veterans Health Administration (VHA) national database was queried for subjects between 1999 and 2017 with ICD-9/-10 diagnosis code for GCA, procedure code for TAB, and ICD-9/-10 diagnosis code for blindness, anterior or posterior ischemic optic neuropathy, or branch or central retinal artery occlusion. Pharmacy data regarding prednisone dispensation were collected. A Cox proportional hazard model was performed using ophthalmic complication by 1 year as the outcome variable in TAB-negative subjects, adjusting for age, TAB length, TAB laterality, and prednisone dose relative to GCA diagnosis date.
 
  Incident ophthalmic complication occurred by 1 year in 9.6% with positive TAB and in 6.2% with ne accrued an incident ICD-9/-10 code for ophthalmologic complication within a year after diagnosis, most occurring within the first month. Delaying prednisone initiation 14-28 days after GCA diagnosis in TAB-negative subjects led to a 3.5-fold higher rate of ophthalmic events occurring by 1 year.  https://www.selleckchem.com/products/dorsomorphin-2hcl.html  Key Points • This study provides an incidence rate of ophthalmic complication by one year in biopsy-negative subjects suspected of having GCA. • Delaying prednisone initiation 14-28 days after GCA diagnosis in TAB-negative GCA subjects led to a 3.5-fold higher rate of ophthalmic events occurring by 1 year.The 22q11.2 deletion syndrome (22q11DS) is associated with a wide spectrum of cognitive and psychiatric symptoms. Despite the considerable work performed over the past 20 years, the genetic etiology of the neurodevelopmental phenotype remains speculative. Here, we report de novo heterozygous truncating variants in the HIRA (Histone cell cycle regulation defective, S. Cerevisiae, homolog of, A) gene associated with a neurodevelopmental disorder in two unrelated patients. HIRA is located within the commonly deleted region of the 22q11DS and encodes a histone chaperone that regulates neural progenitor proliferation and neurogenesis, and that belongs to the WD40 Repeat (WDR) protein family involved in brain development and neuronal connectivity. To address the specific impact of HIRA haploinsufficiency in the neurodevelopmental phenotype of 22q11DS, we combined Hira knock-down strategies in developing mouse primary hippocampal neurons, and the direct study of brains from heterozygous Hira+/- mice. Our in vitro analyses revealed that Hira gene is mostly expressed during neuritogenesis and early dendritogenesis stages in mouse total brain and in developing primary hippocampal neurons. Moreover, shRNA knock-down experiments showed that a twofold decrease of endogenous Hira expression level resulted in an impaired dendritic growth and branching in primary developing hippocampal neuronal cultures. In parallel, in vivo analyses demonstrated that Hira+/- mice displayed subtle neuroanatomical defects including a reduced size of the hippocampus, the fornix and the corpus callosum. Our results suggest that HIRA haploinsufficiency would likely contribute to the complex pathophysiology of the neurodevelopmental phenotype of 22q11DS by impairing key processes in neurogenesis and by causing neuroanatomical defects during cerebral development.