External fixation was used in the treatment of 154 intertrochanteric fractures of the femur over a period of eight years. Good fixation and early ambulation was achieved in all cases. Blood loss was slight. There were 12 deaths due to medical causes unrelated to the surgical procedure. Deep pin-track infection occurred in six cases and late displacement of the fracture fragments in nine. The average time for union was 16 weeks. The technique is simple, quick and inexpensive, and causes minimal surgical trauma. All these features are particularly relevant where resources are limited.

Lithium is an effective, well-established treatment for bipolar disorder (BD). However, the mechanisms of its action, and reasons for variations in clinical response, are unclear. We used neural precursor cells (NPCs) and lymphoblastoid cell lines (LCLs), from BD patients characterized for clinical response to lithium (using the “Alda scale” and “NIMH Retrospective Life chart method”), to interrogate cellular phenotypes related to both disease and clinical lithium response. NPCs from two biologically related BD patients who differed in their clinical response to lithium were compared with healthy controls. RNA-Seq and analysis, mitochondrial membrane potential (MMP), cell viability, and cell proliferation parameters were assessed, with and without in vitro lithium. These parameters were also examined in LCLs from 25 BD patients (16 lithium responders and 9 non-responders), and 12 controls. MMP was lower in both NPCs and LCLs from BD; but it was reversed with in vitro lithium only in LCLs, and this was unrelated to clinical lithium response. The higher cell proliferation observed in BD was unaffected by in vitro lithium. Cell death was greater in BD. However, LCLs from clinical lithium responders could be rescued by addition of in vitro lithium. In vitro lithium also enhanced BCL2 and GSK3B expression in these cells. Our findings indicate cellular phenotypes related to the disease (MMP, cell proliferation) in both NPCs and LCLs; and those related to clinical lithium response (cell viability, BCL2/GSK3B expression) in LCLs.

Absence of patella as an isolated anomaly is extremely rare. It is usually absent as part of a syndrome, most commonly hereditary arthro-onchyo-dysplasia (Nail Patella Syndrome). We present a case of congenital bilateral absence of patella in a nine-year-old boy with no associated anomalies.

Context: Physical activity has shown to be beneficial for the overall physical and mental health of youth. There has been an increasing focus on youth sports moving from a recreational activity to becoming a launching pad for participation at elite levels. Several models of athlete development have emerged to guide specialized and nonspecialized athletes at an age-appropriate level, taking into consideration their physical and mental development. The purpose of this review is to summarize the current evidence and theoretical models regarding youth athlete development and discuss broader initiatives for sports participation and future directions for the field. Evidence Acquisition: An electronic databases search, including PubMed, Google Scholar, ScienceDirect, National Institutes of Health, UpToDate, and Springer was conducted. Articles from 1993 to 2021 were included. The search terms long term athlete development, LTAD model, youth physical development, youth athlete development, sports specialization, and pediatric athlete, among others, were used. Study Design: Narrative review. Level of Evidence: Levels 4 and 5. Results: Several models of youth athlete development are discussed in this article. More recent models have built on previous models to incorporate more age- and development-specific recommendations; however, no singular model could be identified as the gold standard for youth athlete development, especially given the lack of empirical data to support these models. Conclusion: Youth athlete development currently consists of several theoretical models, each with their own strengths and weaknesses, that can guide the training of young athletes to maximize their performance. Those involved in this process—physicians, athletic trainers, coaches, physical educators, and parents—should understand these various models and trial their various features to see what works best for their individual athlete with consideration given to factors such as their stage of development. Ultimately, more empirical data are required to definitively state which is the optimal approach.

Aim Severe mental illnesses (SMI), such as bipolar disorder and schizophrenia, are highly heritable, and have a complex pattern of inheritance. Genome‐wide association studies detect a part of the heritability, which can be attributed to common genetic variation. Examination of rare variants with next‐generation sequencing may add to the understanding of the genetic architecture of SMI. Methods We analyzed 32 ill subjects from eight multiplex families and 33 healthy individuals using whole‐exome sequencing. Prioritized variants were selected by a three‐step filtering process, which included: deleteriousness by five in silico algorithms; sharing within families by affected individuals; rarity in South Asian sample estimated using the Exome Aggregation Consortium data; and complete absence of these variants in control individuals from the same gene pool. Results We identified 42 rare, non‐synonymous deleterious variants (~5 per pedigree) in this study. None of the variants were shared across families, indicating a ‘private’ mutational profile. Twenty (47.6%) of the variant harboring genes were previously reported to contribute to the risk of diverse neuropsychiatric syndromes, nine (21.4%) of which were of Mendelian inheritance. These included genes carrying novel deleterious variants, such as the GRM1 gene implicated in spinocerebellar ataxia 44 and the NIPBL gene implicated in Cornelia de Lange syndrome. Conclusion Next‐generation sequencing approaches in family‐based studies are useful to identify novel and rare variants in genes for complex disorders like SMI. The findings of the study suggest a potential phenotypic burden of rare variants in Mendelian disease genes, indicating pleiotropic effects in the etiology of SMI.