Glioblastoma multiforme (GBM) is a highly malignant type of brain tumor found in humans. GBM cells reproduce quickly, and the median survival time for patients after therapy is approximately 1 year with a high relapse rate. Current therapies and diagnostic tools for GBM are limited; therefore, we searched for a more favorable therapeutic target or marker protein for both therapy and diagnosis. We used mass spectrometry (MS) analysis to identify GBM‐associated marker proteins from human plasma and GBM cell cultures. Additional plasma and 52 brain tissues obtained from patients with gliomas were used to validate the association rate of serum amyloid A1 (SAA1) in different grades of gliomas and its distribution in tumors. Microarray database analysis further validated the coefficient of SAA1 levels in gliomas. The cellular mechanisms of SAA1 in GBM proliferation and infiltration were investigated in vitro. We analyzed the correlation between SAA1 and patients' medication requirement to demonstrate the clinical effects of SAA1 in GBM. SAA1 was identified from MS analysis, and its level was revealed to be correlated with the disease grade, clinical severity, and survival rate of patients with gliomas. In vitro cultures, including GBM cells and normal astrocytes, revealed that SAA1 promotes cell migration and invasion through integrin αVβ3 to activate the Erk signaling pathway. Magnetic resonance imaging and tumor region‐specific microarray analysis identified a correlation between SAA1 and GBM cell infiltration in patients. In summary, our results demonstrate that SAA1 in combination with integrin αV and β3 can serve as an indicator of high glioblastoma risk. We also identified the cellular mechanisms of SAA1 contributing to GBM progression, which can serve as the basis for future GBM therapy.

Chondrocytes and osteoblasts differentiated from induced pluripotent stem cells (iPSCs) will provide insights into skeletal development and genetic skeletal disorders and will generate cells for regenerative medicine applications. Here, we describe a method that directs iPSC-derived sclerotome to chondroprogenitors in 3D pellet culture then to articular chondrocytes or, alternatively, along the growth plate cartilage pathway to become hypertrophic chondrocytes that can transition to osteoblasts. Osteogenic organoids deposit and mineralize a collagen I extracellular matrix (ECM), mirroring in vivo endochondral bone formation. We have identified gene expression signatures at key developmental stages including chondrocyte maturation, hypertrophy, and transition to osteoblasts and show that this system can be used to model genetic cartilage and bone disorders.

The use of blood plasma biomarkers in gastric cancer (GC) management is limited due to a lack of reliable biomarkers. An LC‐MS/MS assay and a bioinformatic analysis were performed to identify blood plasma biomarkers in a GC discovery cohort. The data obtained were verified and validated by western blotting and an ELISA in an independent study cohort. A label‐free quantification analysis of the MS data using PEAKS7 software found that four plasma proteins of apolipoprotein C‐1, gelsolin, sex hormone‐binding globulin (SHBG), and complement component C4‐A were significantly overexpressed in GC patients. A western blot assay of these plasma proteins showed that only SHBG was consistently overexpressed in the patient group. ELISA measurement of SHBG blood plasma levels confirmed that the patient group had significantly higher SHBG levels than the control group. SHBG levels in the patient group remained significantly higher after being stratified by gender, age, and disease stage. These findings show that LC‐MS/MS is powerful and highly sensitive for plasma biomarker discovery, and SHBG could be a potential plasma biomarker for GC management.

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Occupational skin-related problems include dermatoses caused by agents in the working environment. For health care workers, these occupational dermatoses could be due to usage of personal protective equipment (PPE), such as gloves, masks, goggles, and other protective equipment. These PPE contribute to both allergic and irritant contact dermatitis. This review summarized the skin damage after PPE usage and hand hygiene protocol. Recommendations should be established to prevent these occupational dermatoses from PPE usage.

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BACKGROUND The COVID-19 is an emerging disease that commonly involves respiratory complaints, including acute respiratory distress syndrome. The effect of COVID-19 on pulmonary function is still unclear and only based on sporadic reports with a small sample size. This study aimed to compile evidence on the pulmonary function of patients who have recovered from COVID-19. METHODS Literature searching was conducted in PubMed, Embase, Google Scholar, Scopus, Web of Sciences, and CINAHL. Any types of studies published before June 26, 2020 and reported lung function tests of post-COVID-19 patients were included. Articles reporting data from early hospitalization were excluded. The risk of bias was measured using tools developed by the Joanna Briggs Institute. Meta-analysis was done using a meta statistical package in R and presented in the random effects model. RESULTS 378 recovered COVID-19 patients in 7 studies were included. The lung function measurement periods were varied, ranging from 14 days after hospitalization to 10 weeks after receiving rehabilitation. Meta-analyses found that the pooled mean of diffusion capacity of carbon monoxide in recovered COVID-19 patients was lower than 80% predicted, whereas the other parameters were normal. The forced vital capacity and total lung capacity showing restrictive lung disorders were significantly lower in the severe COVID-19 survivors. CONCLUSIONS COVID-19 has a negative impact on lung function for at least several weeks in the recovery period. Diffusion and restrictive problems could be the main long-term consequences of COVID-19.

Background Mutations in the a-subunit of the first neuronalsodium channel gene SCNIA have been demonstrated forgeneralized epilepsy \\lith febrile seizures plus (GEFS+), severemyoclonic epilepsy in infancy (SMEI), and borderline SMEI(SMEB). SCNIA mutations are also described in patients 'Withpsychiatric disorders such as autism.Objective To identify the mutations of SCNIA gene in patientswith GEFS+ spectrum which may be related to autism.Methods We examined four patients v.ith autism and GEFS+spectrum who were admitted to the Department of Child Health,Sardjito Hospital, Yogyakarta, Indonesia. Diagnosis of autism wasbased on DSM􀁟IV;ICD X criteria. Mutations in SCNIA wereidentified by PCRamplification and denaturing high􀁟performanceliquid chromatography analysis, Mth subsequent sequencing.Results There were four patients, all boys, aged 1.8 year to 7 years.The phenotypes of epilepsy were GEFS+ in one patient, SMEBin one patient and SMEI in two patients. Sequencing analysisrevealed a G􀁟to􀁟A heterozygous transition which was detectedat nucleotide c.4834G>A (p.V1612I ) in exon 25. Other singlenucleotid polymorphisms (SNPs) were c.383 +66T>C in intron 2,c.603-91G>A and c.603-1060> T in intron 4, c.965-21C> T inintron 6, c.1028+21T>Cin intron 7, c.2173G>A in exon 12 andc. 2177-38C>A, c.2177-12delT, c.2176+44C> T in intron 12.Conclusion In this study, we reported the first cases Mth mutationin SCNIA gene in GEFS+ spectrum related to autistic patientsin Indonesian population, which showed a missense mutationp.V16121. [Paediatr lndones. 2010;50:125-32].