Numerous drugs have been linked to the induction or exacerbation of systemic cutaneous lupus erythematosus (SCLE). This report presents the third case of the biologic abatacept as an exacerbating medication for SCLE. A 73-year old woman with a remote history of subacute cutaneous lupus and rheumatoid arthritis, well controlled on hydroxychloroquine, presented with worsening annular erythematous, slightly scaly plaques on her forearms and hands. She had been started on abatacept a month prior. She was diagnosed with SCLE exacerbated by abatacept given the clinical findings, time course, and skin biopsy with interface dermatitis. Her skin eruption cleared completely several months later after discontinuing abatacept and switching to tociluzumab, while remaining on hydroxychloroquine. This case highlights the need to consider abatacept as a potential exacerbating medication for SCLE in any patient with a new photodistributed papulosquamous eruption.The frequent finding of thrombocytopenia in patients with severe SARS-CoV-2 infection (COVID-19) and previous evidence that several viruses enter platelets suggest that SARS-CoV-2 might be internalized by platelets of COVID-19.  https://www.selleckchem.com/products/AZD2281(Olaparib).html  Aim of our study was to assess the presence of SARS-CoV-2 RNA in platelets from hospitalized patients with aconfirmed diagnosis of COVID-19. RNA was extracted from platelets, leukocytes and serum from 24 COVID-19 patients and 3 healthy controls, real-time PCR and ddPCR for viral genes were carried out. SARS-CoV-2 RNA was not detected in any of the samples analyzed nor in healthy controls, by either RT-PCR or ddPCR, while RNA samples from nasopharyngeal swabs of COVID-19 patients were correctly identified. Viral RNA was not detected independently of viral load, of positive nasopharyngeal swabs, or viremia, the last detected in only one patient (4.1%). SARS-CoV-2 entry in platelets is not acommon phenomenon in COVID-19 patients, differently from other viral infections.
  To assess the empirical evidence for the treatment of attention deficit/hyperactivity disorder (ADHD) in populations with autism spectrum disorder (ASD).
 
  A systemic PubMed, PsychINFO, Embase, and Medline database search of peer-reviewed literature was conducted. Included in the review were controlled trials published in English with sample sizes ⩾10 participants examining the safety and efficacy of anti-ADHD medication in ASD populations. Data was extracted on relevant variables of study design, demographics, associated psychopathology, medication dose, efficacy, and tolerability.
 
  Nine controlled trials met the inclusion and exclusion criteria five with methylphenidate, three with atomoxetine, and one with guanfacine. Sample sizes ranged from 10 to 128 with 430 children participating across all the trials. In all the trials, treatment response was significantly superior to placebo. However, almost all trials assessed only hyperactivity, and most included only participants with intellectual disability wividuals with ASD and in adults. Response to ADHD medications in ASD were adversely moderated by the presence of intellectual disability and mood lability.
  Femoral head collapse and coxa vara lead to internal fixator failure in elderly patients with hip fracture. External fixator application is an optimal choice; however, the existing methods have many disadvantages.
 
  Type 31-A1.3 hip fracture models were developed in nine pairs of 1-year-old fresh bovine corpse femur specimens. Each left femur specimen was fixed by a dynamic hip screw (control group), and each right femur specimen was fixed by the slide-poking external fixator (experimental group). Vertical loading and torsion tests were then performed in both groups.
 
  In the vertical loading experiment, a 1000-N load was implemented. The mean vertical downward displacement of the femoral head in the experimental and control groups was 1.49322 ± 0.116280 and 2.13656 ± 0.166374 mm, respectively. In the torsion experiment, when the torsion was increased to 10.0 Nm, the mean torsion angle in the experimental and control groups was 7.9733° ± 1.65704° and 15.4889° ± 0.73228°, respectively. The slide-poking external fixator was significantly more resistant to compression and rotation than the dynamic hip screw.
 
  The slide-poking external fixator for hip fractures that was designed and developed in this study can provide sufficient stability to resist compression and rotation in hip fractures.
 The slide-poking external fixator for hip fractures that was designed and developed in this study can provide sufficient stability to resist compression and rotation in hip fractures.Cadmium (Cd) has a direct toxic effect on bones. Statins such as simvastatin have protective effects on various diseases, including on tissue injury. The current study revealed the efficacy of simvastatin on Cd-induced preosteoblast injury. Preosteoblast MC3T3-E1 cells were incubated with various doses of CdCl2 for 12 h, 24 h and 48 h, and then the cell cytotoxicity was assessed using MTT assay and flow cytometry, respectively. The expression level of Nox4 was assessed by Western blot and qRT-PCR. The morphological appearance of MC3T3-E1 cells was observed under a microscope. Cells exposed to CdCl2 (5 µM) were further treated by simvastatin at various doses, subsequently cell viability, apoptosis and the expression of Nox4 were measured. Furthermore, to confirm the protective effects of simvastatin on Cd-induced pre-osteoblast injury, functional rescue assays were performed after corresponding cell treatment by simvastatin (10-8 M), CdCl2 (5 µM), and overexpression of Nox4. Expressions of cell apoptosis-related markers were measured by Western blot and qRT-PCR. The results revealed that CdCl2 caused MC3T3-E1 cell injury because the cell viability was decreased and the apoptosis was increased. Nox4 expression was up-regulated with the increase of CdCl2 concentrations. Simvastatin increased the cell viability, relieved the cell apoptosis and Nox4 expression previously increased by CdCl2. The effects of CdCl2 on MC3T3-E1 cells and Nox4 expression could be attenuated by simvastatin, and promoted by Nox4 overexpression. The current study found that simvastatin protects Cd-induced preosteoblast injury via Nox4, thus, it can be used as a potential drug for treating cadmium-induced bone injury.