Investigation of the Microstructure and Compressibility of Biodegradable Fe-Mn-Cu/W/Co Nanostructured Alloy Powders Synthesized by Mechanical Alloying

In this research work, the nanostructured Fe-Mn (BM0), Fe-Mn-Cu (BM1), Fe-Mn-W (BM2), and Fe-Mn-Co (BM3) biodegradable alloys were successfully synthesized using mechanical alloying. The microstructure of the synthesized alloys was examined using XRD, SEM equipped with EDS, and HRTEM techniques. The results obtained based on these techniques confirmed the development of nanostructured BM0, BM1, BM2, and BM3 alloys and homogenous solid solutions with an even elemental dispersion. The compressibility of the synthesized alloys was investigated experimentally and empirically in the as-milled conditions and after applying a stress relief treatment (150 °C for 1 h). The load applied for compaction experiments ranged from 25–1100 MPa with a rate of 1 mm/min. According to the experimentation performed in the current study, the relative density of the as-milled BM0, BM1, BM2, and BM3 alloys was 72.90% and 71.64%, 72.32%, and 72.03%, respectively. After applying the stress relief treatment, the density was observed to increase to 75.23%, 77.10%, 72.65%, and 72.86% for BM0-S, BM1-S, BM2-S and BM3-S samples, respectively. A number of compaction models were tested to identify the optimum models for predicting the compressibility behavior of nanostructured Fe-Mn, Fe-Mn-Cu, Fe-Mn-W, and Fe-Mn-Co alloys in the as-milled and stress-relieved conditions.     

Stand-alone renal SLICC criterion with full house glomerular deposits: is it enough for childhood lupus nephritis?

Clinical Rheumatology - The objective of this study is to assess the usefulness of the stand-alone renal SLICC criterion in patients with childhood systemic lupus erythematosus (cSLE) and report...     

Traumatic retropulsion of T10 vertebra in a 5-year-old boy with involvement of neurocentral synchondrosis: a case report and review of the literature

Study design

This is a case report of a traumatic retropulsion of the T10 vertebral body in a 5-year-old boy.

Objectives

This paper aims to describe a rare pediatric fracture where there was involvement of the neurocentral synchondrosis (NCS) and to evaluate the characteristics of this type of fractures in children.

Summary of background data

The NCS is the junction between the vertebral body and the pedicle bilaterally where the vertebra grows horizontally. It closes between 11 and 16 years. It is a known location for spine fracture. However, it was mainly reported in children less than 2 years of age secondary to nontraumatic injury and at the junction levels of the spine. This is the first case of a fracture involving the NCS in a child older than 2 years, due to trauma, and in a non-junctional area of the spine.

Methods

This 5-year-old boy was involved in a motor vehicle collision where he was ejected from the car. He had bilateral lower limb paresthesia and weakness. The fracture involved the neurocentral synchondrosis on the left side and impacted the vertebral body into the pedicle on the right side. Additionally, there was posterior vertebral element injury. He was treated with wide laminectomy and posterior pedicle screw instrumentation.

Results

At 18 months of follow-up, the patient showed a normal neurologic status and a normal alignment of the spine.

Conclusion

Traumatic retropulsion of the thoracic spine with involvement of the NCS is possible in young age when exposed to a significant trauma. Restoration of spine alignment and normal neurological function could be achieved with a single posterior approach.

Key points

- Pediatric fractures are uncommon and tend to affect junction areas. - A fracture through the neurocentral synchondrosis is possible before the age of closure (11–16 years) with forcible trauma. - Single posterior decompression and instrumented fusion is sufficient to restore alignment and neurological function.     

EMC10 homozygous variant identified in a family with global developmental delay,mild intellectual disability,and speech delay

In recent years, several genes have been implicated in the variable disease presentation of global developmental delay (GDD) and intellectual disability (ID). The endoplasmic reticulum membrane protein complex (EMC) family is known to be involved in GDD and ID. Homozygous variants of EMC1 are associated with GDD, scoliosis, and cerebellar atrophy, indicating the relevance of this pathway for neurogenetic disorders. EMC10 is a bone marrow-derived angiogenic growth factor that plays an important role in infarct vascularization and promoting tissue repair. However, this gene has not been previously associated with human disease. Herein, we describe a Saudi family with two individuals segregating a recessive neurodevelopmental disorder. Both of the affected individuals showed mild ID, speech delay, and GDD. Whole-exome sequencing (WES) and Sanger sequencing were performed to identify candidate genes. Further, to elucidate the functional effects of the variant, quantitative real-time PCR (RT-qPCR)-based expression analysis was performed. WES revealed a homozygous splice acceptor site variant (c.679-1G>A) in EMC10 (chromosome 19q13.33) that segregated perfectly within the family. RT-qPCR showed a substantial decrease in the relative EMC10 gene expression in the patients, indicating the pathogenicity of the identified variant. For the first time in the literature, the EMC10 gene variant was associated with mild ID, speech delay, and GDD. Thus, this gene plays a key role in developmental milestones, with the potential to cause neurodevelopmental disorders in humans.     

Nuclear FABP7 regulates cell proliferation of wild‐type IDH1 glioma through caveolae formation

Isocitrate dehydrogenase 1 (IDH1) is a key enzyme in cellular metabolism. IDH1 mutation (IDH1mut) is the most important genetic alteration in lower grade glioma, whereas glioblastoma (GB), the most common malignant brain tumor, often has wild‐type IDH1 (IDH1wt). Although there is no effective treatment yet for neither IDH1wt nor IDHmut GB, it is important to note that the survival span of IDH1wt GB patients is significantly shorter than those with IDH1mut GB. Thus, understanding IDH1wt GB biology and developing effective molecular‐targeted therapies is of paramount importance. Fatty acid‐binding protein 7 (FABP7) is highly expressed in GB, and its expression level is negatively correlated with survival in malignant glioma patients; however, the underlying mechanisms of FABP7 involvement in tumor proliferation are still unknown. In this study, we demonstrate that FABP7 is highly expressed and localized in nuclei in IDH1wt glioma. Wild‐type FABP7 (FABP7wt) overexpression in IDH1wt U87 cells increased cell proliferation rate, caveolin‐1 expression, and caveolae/caveosome formation. In addition, FABP7wt overexpression increased the levels of H3K27ac on the caveolin‐1 promoter through controlling the nuclear acetyl‐CoA level via the interaction with ACLY. Consistent results were obtained using a xenograft model transplanted with U87 cells overexpressing FABP7. Interestingly, in U87 cells with mutant FABP7 overexpression, both in vitro and in vivo phenotypes shown by FABP7wt overexpression were disrupted. Furthermore, IDH1wt patient GB showed upregulated caveolin‐1 expression, increased levels of histone acetylation, and increased levels of acetyl‐CoA compared with IDH1mut patient GB. Taken together, these data suggest that nuclear FABP7 is involved in cell proliferation of GB through caveolae function/formation regulated via epigenetic regulation of caveolin‐1, and this mechanism is critically important for IDH1wt tumor biology.