Segond's fracture: a biomechanical cadaveric study using navigation

Background Segond’s fracture is a well-recognised radiological sign of an anterior cruciate ligament (ACL) tear. While previous studies evaluated the role of the anterolateral ligament (ALL) and complex injuries on rotational stability of the knee, there are no studies on the biomechanical effect of Segond’s fracture in an ACL deficient knee. The aim of this study was to evaluate the effect of a Segond’s fracture on knee rotation stability as evaluated by a navigation system in an ACL deficient knee. Materials and methods Three different conditions were tested on seven knee specimens: intact knee, ACL deficient knee and ACL deficient knee with Segond’s fracture. Static and dynamic measurements of anterior tibial translation (ATT) and axial tibial rotation (ATR) were recorded by the navigation system (2.2 OrthoPilot ACL navigation system B. Braun Aesculap, Tuttlingen, Germany). Results Static measurements at 30 showed that the mean ATT at 30 of knee flexion was 5.1 ± 2.7 mm in the ACL intact condition, 14.3 ± 3.1 mm after ACL cut (P = 0.005), and 15.2 ± 3.6 mm after Segond’s fracture (P = 0.08). The mean ATR at 30 of knee flexion was 20.7 ± 4.8 in the ACL intact condition, 26.9 ± 4.1 in the ACL deficient knee (P[0.05) and 30.9 ± 3.8 after Segond’s fracture (P = 0.005). Dynamic measurements during the pivot-shift showed that the mean ATT was 7.2 ± 2.7 mm in the intact knee, 9.1 ± 3.3 mm in the ACL deficient knee(P = 0.04) and 9.7 ± 4.3 mm in the ACL deficient knee with Segond’s fracture (P = 0.07). The mean ATR was 9.6 ± 1.8 in the intact knee, 12.3 ± 2.3 in the ACL deficient knee (P[0.05) and 19.1 ± 3.1 in the ACL deficient knee with Segond’s lesion (P = 0.016). Conclusion An isolated lesion of the ACL only affects ATT during static and dynamic measurements, while the addition of Segond’s fracture has a significant effect on ATR in both static and dynamic execution of the pivot-shift test, as evaluated with the aid of navigation

Synthesis of Nanofiltration Membrane Developed from Triethanolamine (TEOA) and Trimesoyl Chloride (TMC) for Separation of Xylose from Glucose

Synthesis of thin film composite (TFC) nanofilt ration (NF) membrane has experienced tremendous development since the concept of interfacial polymerisation (IP) was first introduced. One of its new application is on the separation of xylose from glucos e in biomass hydrolysate. In this present study, NF TFC membrane has been produced through interfacial poly merisation by manipulation the concentration of triethanolamine (TEOA) at 35 min reaction time with 0. 15 % w/v of trimesoyl chloride (TMC). The membrane was then characterised in term of their chemical and physical properties, and separation performance between xylose and glucose. The growth of thin layer f ilm depends on concentration of TEOA as the monomer and reaction time. As concentration of TEOA and re action time increased, the layer of the TFC becomes thicker thus decreases the permeability of the membrane. Contradicted to this study, the lowest and the highest permeability were recorded at 4 % w/v of TEOA and 8 % w/v of TEOA at reaction time of 35-min in TMC. The TFC membrane prepared with 4 % w/v TEOA has high in permeate flux, resultant in high xylose separation of 1.3. Low permeate flux but moderate xylose separation factor of 0.93 was obtained for the TFC membrane prepared with 8 % w/v TEOA

Extensive unusual lesions on a large number of immersed human victims found to be from cookiecutter sharks (Isistius spp.): an examination of the Yemenia plane crash.

Accurate determination of the origin and timing of trauma is key in medicolegal investigations when the cause and manner of death are unknown. However, distinction between criminal and accidental perimortem trauma and postmortem modifications can be challenging when facing unidentified trauma. Postmortem examination of the immersed victims of the Yemenia airplane crash (Comoros, 2009) demonstrated the challenges in diagnosing extensive unusual circular lesions found on the corpses. The objective of this study was to identify the origin and timing of occurrence (peri- or postmortem) of the lesions.A retrospective multidisciplinary study using autopsy reports (n = 113) and postmortem digital photos (n = 3 579) was conducted. Of the 113 victims recovered from the crash, 62 (54.9 %) presented unusual lesions (n = 560) with a median number of 7 (IQR 3 ∼ 13) and a maximum of 27 per corpse. The majority of lesions were elliptic (58 %) and had an area smaller than 10 cm2 (82.1 %). Some lesions (6.8 %) also showed clear tooth notches on their edges. These findings identified most of the lesions as consistent with postmortem bite marks from cookiecutter sharks (Isistius spp.). It suggests that cookiecutter sharks were important agents in the degradation of the corpses and thus introduced potential cognitive bias in the research of the cause and manner of death. A novel set of evidence-based identification criteria for cookiecutter bite marks on human bodies is developed to facilitate more accurate medicolegal diagnosis of cookiecutter bites.This is the final version of the article. It first appeared from Springer via http://dx.doi.org/10.1007/s00414-016-1449-

Joint Belgian recommendation on screening for DPD-deficiency in patients treated with 5-FU, capecitabine (and tegafur)

Objectives: Fluoropyrimidines such as 5-Fluorouracil (5-FU), capecitabine and tegafur are drugs that are often used in the treatment of maliginancies. The enzyme dihydropyrimidine dehydrogenase (DPD) is the first and rate limiting enzyme of 5-FU catabolism. Genetic variations within the DPYD gene (encoding for DPD protein) can lead to reduced or absent DPD activity. Treatment of DPD deficient patients with fluoropyrimidines can result in severe and, rarely, fatal toxicity. Screening for DPD deficiency should be implemented in practice. Methods: The available methods in routine to screen for DPD deficiency were analyzed and discussed in several group meetings involving members of the oncological, genetic and toxicological societies in Belgium: targeted genotyping based on the detection of 4 DPYD variants and phenotyping, through the measurement of uracil and dihydrouracil/uracil ratio in plasma samples. Results: The main advantage of targeted genotyping is the existence of prospectively validated genotype-based dosing guidelines. The main limitations of this approach are the relatively low sensitivity to detect total and partial DPD deficiency and the fact that this approach has only been validated in Caucasians so far. Phenotyping has a better sensitivity to detect total and partial DPD deficiency when performed in the correct analytical conditions and is not dependent on the ethnic origin of the patient. Conclusion: In Belgium, we recommend phenotype or targeted genotype testing for DPD deficiency before starting 5-FU, capecitabine or tegafur. We strongly suggest a stepwise approach using phenotype testing upfront because of the higher sensitivity and the lower cost to society

Hydroxychloroquine in a G6PD-Deficient Patient with COVID-19 Complicated by Haemolytic Anaemia: Culprit or Innocent Bystander?

Hydroxychloroquine has been used worldwide as a first-line treatment for patients hospitalized with COVID-19. Little is known about COVID-19 and its effects on patients with congenital red blood cell disorders. We report a case of haemolytic anaemia in a 32-year-old patient and a fortuitous highlighting of G6PD deficiency. We reviewed the literature to assess the risk of hydroxychloroquine use in this context

GWAS META-analysis followed by MENDELIAN randomisation revealed potential control mechanisms for circulating α-klotho levels

The protein α-Klotho acts as transmembrane co-receptor for fibroblast growth factor 23 (FGF23) and is a key regulator of phosphate homeostasis. However, α-Klotho also exists in a circulating form, with pleiotropic, but incompletely understood functions and regulation. Therefore, we undertook a genome-wide association study (GWAS) meta-analysis followed by Mendelian randomization (MR) of circulating α-Klotho levels. Plasma α-Klotho levels were measured by enzyme-linked immunosorbent assay (ELISA) in the Ludwigshafen Risk and Cardiovascular Health and Avon Longitudinal Study of Parents and Children (mothers) cohorts, followed by a GWAS meta-analysis in 4376 individuals across the two cohorts. Six signals at five loci were associated with circulating α-Klotho levels at genome-wide significance (P 9% of the variation in circulating α-Klotho levels. MR analyses revealed no causal relationships between α-Klotho and renal function, FGF23-dependent factors such as vitamin D and phosphate levels, or bone mineral density. The screening for genetic correlations with other phenotypes followed by targeted MR suggested causal effects of liability of Crohn’s disease risk [Inverse variance weighted (IVW) beta = 0.059 (95% confidence interval 0.026, 0.093)] and low-density lipoprotein cholesterol levels [−0.198 (−0.332, −0.063)] on α-Klotho. Our GWAS findings suggest that two enzymes involved in post-translational modification, B4GALNT3 and CHST9, contribute to genetic influences on α-Klotho levels, presumably by affecting protein turnover and stability. Subsequent evidence from MR analyses on α-Klotho levels suggest regulation by mechanisms besides phosphate-homeostasis and raise the possibility of cross-talk with FGF19- and FGF21-dependent pathways, respectively. Significance statement: α-Klotho as a transmembrane protein is well investigated along the endocrine FGF23-α-Klotho pathway. However, the role of the circulating form of α-Klotho, which is generated by cleavage of transmembrane α-Klotho, remains incompletely understood. Genetic analyses might help to elucidate novel regulatory and functional mechanisms. The identification of genetic factors related to circulating α-Klotho further enables MR to examine causal relationships with other factors. The findings from the first GWAS meta-analysis of circulating α-Klotho levels identified six genome-wide significant signals across five genes. Given the function of two of the genes identified, B4GALNT3 and CHST9, it is tempting to speculate that post-translational modification significantly contributes to genetic influences on α-Klotho levels, presumably by affecting protein turnover and stability

Anatomic and histological study of the anterolateral aspect of the knee: a SANTI Group investigation

Background: The structure and function of the anterolateral aspect of the knee have been significantly debated, with renewed interest in this topic since the description of the anterolateral ligament (ALL). Purpose: To define and describe the distinct structures of the lateral knee and to correlate the macroscopic and histologic anatomic features. Study Design: Descriptive laboratory study. Methods: Twelve fresh-frozen human cadavers were used for anatomic analysis. In the left knee, a layer-by-layer dissection and macroscopic analysis were performed. In the right knee, an en bloc specimen was obtained encompassing an area from the Gerdy tubercle to the posterior fibular head and extending proximally from the anterior aspect to the posterior aspect of the lateral femoral epicondyle. The en bloc resection was then frozen, sliced at the level of the joint line, and reviewed by a musculoskeletal pathologist. Results: Macroscopically, the lateral knee has 4 main layers overlying the capsule of the knee: the aponeurotic layer, the superficial layer including the iliotibial band (ITB), the deep fascial layer, and the ALL. Histologically, 8 of 12 specimens demonstrated 4 consistent, distinct structures: the ITB, the ALL, the lateral collateral ligament, and the meniscus. Conclusion: The lateral knee has a complex orientation of layers and fibers. The ALL is a distinct structure from the ITB and is synonymous to the previously described capsulo-osseous layer of the ITB. Clinical Relevance: Increasingly, lateral extra-articular procedures are performed at the time of anterior cruciate ligament reconstruction. Understanding the anatomic features of the anterolateral aspect of the knee is necessary to understand the biomechanics and function of the structures present and allows surgeons to attempt to replicate those anatomic characteristics when performing extra-articular reconstruction

Hundreds of variants clustered in genomic loci and biological pathways affect human height

Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits, but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait. The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P < 0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways.

The anterolateral ligament of the knee: unwrapping the enigma. Anatomical study and comparison to previous reports.

It has been suggested that the anterolateral ligament (ALL) of the knee may have importance in limiting rotational instability, and reconstruction may prevent a continued pivot-shift following anterior cruciate ligament surgery. However, the anatomy of this ligament has not been consistently reported in recent publications. We describe our experience of cadaveric dissection with reference to other published work.This article is freely available via Open Access. Click on the 'Additional Link' above to access the full-text from the publisher's site.Published (Open Access