The purpose of this study was to report the RNA sequencing profile according to the presence or absence of sarcopenia in elderly patients with osteoporotic hip fracture. Therefore, an important genetic factor candidate for sarcopenia causing hip fracture in elderly with osteoporosis has been identified. The patient group involved subjects over 65 years who had undergone hip fracture surgery. Among 323 hip fracture (HF) patients identified from May 2017 to December 2019, 162 HF patients (90 non-sarcopenia and 72 sarcopenia groups), excluding subjects with high energy trauma and non-osteoporosis, were finally included in the analysis. For RNA sequencing, each patient with hand grip strength (HGS) values in the top 10% were enrolled in the control group and with the bottom 10% in the patient group. After excluding patients with poor tissue quality, 6 patients and 5 patients were selected for sarcopenia and non-sarcopenia groups, respectively. For qPCR validation, each patient with HGS values in the top 20% and bottom 20% was enrolled in the control and patient groups, respectively. After excluding patients with poor tissue quality, 12 patients and 12 patients were enrolled in the sarcopenia and non-sarcopenia groups, respectively. Sarcopenia was defined according to the Asia Working Group for Sarcopenia (AWGS) criteria for low muscle strength (hand grip strength below 18 ​kg in women and 28 ​kg in men) and low muscle mass (SMI below 5.4 ​kg/m2 in women and 7.0 ​kg/m2 in men). The libraries were prepared for 100 bp paired-end sequencing using TruSeq Stranded mRNA Sample Preparation Kit (Illumina, CA, USA). The gene expression counts were supplied to Deseq2 to extract possible gene sets as differentially expressed genes (DEG) that discriminate between sarcopenia and non-sarcopenia groups that were carefully assigned by clinical observation. For the classification of the candidate genes from DEG analysis, we used the public databases; gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Quantitative real-time PCR was performed for validation. Samples collected were subjected to RNAseq using the Illumina platform. A total of 11 samples from both sarcopenia and non-sarcopenia groups were sequenced. Fifteen genes (RUNX 1, NGFR, CH3L1, BCL3, PLA2G2A, MYBPH, TEP1, SEMA6B, CSPG4, ACSL5, SLC25A3, NDUFB5, CYC1, ACAT1, and TCAP) were identified as differentially expressed genes (DEG) in both the groups. In the qPCR results, the expression levels of SLC25A3 and TCAP gene in the OS group were significantly lower than in the non-OS groups whereas an increase in RUNX1 mRNA level was observed in the OS samples (p ​< ​0.05). In summary, this study detected gene expression difference according to the presence or absence of sarcopenia in elderly osteoporosis female patients with hip fracture. We have also identified 15 important genes (RUNX 1, NGFR, CH3L1, BCL3, PLA2G2A, MYBPH, TEP1, SEMA6B, CSPG4, ACSL5, SLC25A3, NDUFB5, CYC1, ACAT1, TCAP), a few GO categories and biological pathways that may be associated with the osteosarcopenia. Our study may provide effective means for the prevention, diagnosis and treatment sarcopenia in elderly osteoporosis female patients. These findings provide a novel insight into the effects of aging on the response in women with postmenopausal osteoporosis. Further studies are underway to identify the specific signalling pathways involved. These results reveal potential therapeutic targets that could aid the regenerative capacity of aging skeletal muscle.

The hallmark symptom of sarcopenia is the loss of muscle mass and strength without the loss of overall body weight. Sarcopenia patients are likely to have worse clinical outcomes and higher mortality than do healthy individuals. The sarcopenia population shows an annual increase of ~0.8% in the population after age 50, and the prevalence rate is rapidly increasing with the recent worldwide aging trend. Based on International Classification of Diseases, Tenth Revision, a global classification of disease published by the World Health Organization, issued the disease code (M62.84) given to sarcopenia in 2016. Therefore, it is expected that the study of sarcopenia will be further activated based on the classification of disease codes in the aging society. Several epidemiological studies and meta-analyses have looked at the correlation between the prevalence of sarcopenia and several environmental factors. In addition, studies using cell lines and rodents have been done to understand the biological mechanism of sarcopenia. Laboratory rodent models are widely applicable in sarcopenia studies because of the advantages of time savings, cost saving, and various analytical applications that could not be used for human subjects. The rodent models that can be applied to the sarcopenia research are diverse, but a simple and fast method that can cause atrophy or aging is preferred. Therefore, we will introduce various methods of inducing muscular atrophy in rodent models to be applied to the study of sarcopenia.

Monoacylglycerol O-acyltransferase 1 (MGAT1) is reported to play a key role in the development of diet-induced nonalcoholic fatty liver disease (NAFLD). Thus, this study investigated the effect of exercise on suppression of the MGAT1 pathway in NAFLD tissue of high-fat diet (HFD)-induced obese rats. Male Sprague-Dawley rats were fed an HFD containing 45% fat for 6 weeks. Upon confirmation that NAFLD had been induced in the obese animals, they were divided into HFD-fed groups provided with exercise (HFD + EXE) or without exercise (HFD) and a group given dietary adjustment (DA) only, for a further 6 weeks of intervention treatment. The 6-week regular moderate aerobic exercise consisted of an accommodation phase with increasing exercise. Lipid accumulation in the liver tissue was determined by Oil Red O staining. The MGAT1 and liver lipogenic gene mRNA levels were measured by qPCR, and their protein levels by western blot assay. Oil Red O staining showed that NAFLD was successfully induced by HFD-fed. The gene expression of MGAT1 was significantly lower in HFD + EXE than HFD. However, there was no significant difference between HFD + EXE and DA. The protein expression of MGAT1 was significantly lower in HFD + EXE than both HFD and DA. Messenger RNA and protein expression of other lipogenic genes were not different among groups. These data indicate that exercise suppresses MGAT1 pathway regardless of HFD feeding; in part, this effect could be greater than DA. Our data suggest that exercise can improve NAFLD, which is probably due to suppression of MGAT1 pathway.

Malarial infection induces tissue hypoxia in the host through destruction of red blood cells. Tissue hypoxia in malarial infection may increase the activity of HIF1α through an intracellular oxygen-sensing pathway. Activation of HIF1α may also induce vascular endothelial growth factor (VEGF) to trigger angiogenesis. To investigate whether malarial infection actually generates hypoxia-induced angiogenesis, we analyzed severity of hypoxia, the expression of hypoxia-related angiogenic factors, and numbers of blood vessels in various tissues infected with Plasmodium berghei. Infection in mice was performed by intraperitoneal injection of 2×106 parasitized red blood cells. After infection, we studied parasitemia and survival. We analyzed hypoxia, numbers of blood vessels, and expression of hypoxia-related angiogenic factors including VEGF and HIF1α. We used Western blot, immunofluorescence, and immunohistochemistry to analyze various tissues from Plasmodium berghei-infected mice. In malaria-infected mice, parasitemia was increased over the duration of infection and directly associated with mortality rate. Expression of VEGF and HIF1α increased with the parasitemia in various tissues. Additionally, numbers of blood vessels significantly increased in each tissue type of the malaria-infected group compared to the uninfected control group. These results suggest that malarial infection in mice activates hypoxia-induced angiogenesis by stimulation of HIF1α and VEGF in various tissues.

Introduction: Trichinella spiralis establishes a chronic infection in skeletal muscle by developing nurse cells within muscle fibers. During symbiosis in host, changes in the muscle fibers and inflammation may affect muscle function.

The endogenous retrovirus (ERV) appeared in the vertebrate genome millions of years ago, but is now inactivated due to mutations such as deletions or nonsense mutations. After the mutation, ERV eventually became fixed in the genome in its endogenous form. In the case of human ERV (HERV), 98 000 ERV elements or fragments were inserted into the human genome, which is approximately 8% of the whole genome.1 HERV is defective and unable to replicate and only traces of the original viruses exist in the human genome.2 Even though HERVs have been reported to be inactive, there are several studies showing the relationship between HERVs and some diseases including cancers. Contreras-Galindo et al 3 first showed that HERV-K genes are significantly upregulated in the plasma of lymphoma and breast cancer patients and that there are virus-like particles in the plasma of lymphoma patients. Many other studies have shown that HERV-K can be a good model for immunotherapeutic targets4 and is a biomarker of early-stage breast cancer.5 Additionally, there have been reports demonstrating that HERV-K is involved in breast cancer,4–⇓6 prostate cancer,7 melanoma8 and ovarian cancer.9 ERV3-1 (HERV-R) is related to lymphoma10 and HERV-E is upregulated in urothelial carcinoma11 and colon cancer.12 We recently reported that the ERV3-1 (HERV-R) env protein is expressed in both adult human organs and tumours using a tissue microarray. We also compared the expression of ERV3-1 between normal and tumour tissues to study the relationship between ERV3-1 and tumour formation. ERV3-1 was highly expressed in certain types of tumours, including lung adenocarcinoma, renal cell carcinoma, papillary carcinoma, hepatocellular carcinoma and adenocarcinoma in the gastrointestinal tract.13 Although …