METHODS: Data from 1,763 Malaysian community-dwelling older persons aged ≥ 60 years were obtained from the LRGS-TUA longitudinal study. Participants were categorized into three groups according to the presence of a single fall (occasional fallers), ≥two falls (recurrent fallers), or absence of falls (non-fallers) at an 18-month follow-up.
RESULTS: Three hundred and nine (17.53 %) participants reported fall occurrences at an 18-month follow-up, of whom 85 (27.51 %) had two or more falls. The incidence rate for occasional and recurrent falls was 8.47 and 3.21 per 100 person-years, respectively. Following multifactorial adjustments, being female (OR: 1.57; 95 % CI: 1.04-2.36), being single (OR: 5.31; 95 % CI: 3.36-37.48), having history of fall (OR: 1.86; 95 % CI: 1.19-2.92) higher depression scale score (OR: 1.10; 95 % CI: 1.02-1.20), lower hemoglobin levels (OR: 0.90; 95 % CI: 0.81-1.00) and lower chair stand test score (OR: 0.93; 95 % CI: 0.87-1.00) remained independent predictors of occasional falls. While, having history of falls (OR: 2.74; 95 % CI: 1.45-5.19), being a stroke survivor (OR: 8.57; 95 % CI: 2.12-34.65), higher percentage of body fat (OR: 1.04; 95 % CI: 1.01-1.08) and lower chair stand test score (OR: 0.87; 95 % CI: 0.77-0.97) appeared as recurrent falls predictors.
CONCLUSIONS: Having history of falls and lower muscle strength were predictors for both occasional and recurrent falls among Malaysian community-dwelling older persons. Modifying these predictors may be beneficial in falls prevention and management strategies among older persons.
METHOD: Cognitive decline was determined by Montreal Cognitive Assessment (MoCA). Oxidative stress markers (malondialdehyde-MDA and superoxide dismutase-SOD) were determined and DNA damage was assayed using Alkaline Comet Assay. Toenail samples were taken and analyzed using ICP-MS to determine trace element levels.
RESULTS: A total of 62.1 % of subjects had cognitive impairment. Subjects with cognitive impairment had significantly higher levels of MDA and DNA damage as compared to the group with normal cognitive function; MDA (2.07 ± 0.05 nmol/L vs 1.85 ± 0.06 nmol/L) (p<0.05) and DNA damage (% Tail Density, 14.52 ± 0.32 vs 10.31 ± 0.42; Tail Moment, 1.79 ± 0.06 vs 1.28 ± 0.06) (p<0.05 for all parameters). However, the level of SOD among subjects with cognitive impairment (6.67 ± 0.33 u.e/min/mg protein) was lower than the level among those with normal cognitive functions (11.36 ± 0.65 u.e/min/mg protein) (p<0.05). Multiple logistic regression revealed the predictors for cognitive impairment among the subjects were DNA damage (Adjusted odd ratio [OR], 1.37; 95% confidence interval [CI], 1.18-1.59), level of trace elements in toenails namely, lead (OR, 2.471; CI, 1.535-3.980) and copper (OR, 1.275; CI, 1.047-1.552) (p<0.05).
CONCLUSION: High levels of lead and copper can lead to increase in oxidative stress levels and are associated with DNA damage that eventually could be associated with cognitive decline.
Aims: This study evaluated the effectiveness of iron supplementation and nutrition education on improving the levels of haemoglobin and ferritin, and decreasing oxidative stress among iron-deficient female adolescents in Gaza, Palestine.
Methods: A total 131 iron-deficient female adolescents were recruited and allocated randomly into 3 different groups. The iron supplementation group (A) received 200 mg of ferrous fumarate weekly during the 3-month intervention, the iron supplementation with nutrition education group (B) received iron supplements with nutrition education sessions, and the control group (C) did not receive any intervention. The levels of haemoglobin, ferritin and malonyl dialdehyde were measured at baseline, after 3 months (at which point the intervention was stopped), and then 3 months later. Trial registration number: ACTRN12618000960257.
Results: Haemoglobin levels increased significantly after supplementation in both groups A and B. At the follow-up stage (3 months after stopping the intervention), iron and haemoglobin levels in group B continued to increase and malonyl dialdehyde decreased. In Group A, haemoglobin, ferritin and malonyl dialdehyde levels decreased after 3 months of stopping the intervention. No changes were seen in Group C.
Conclusions: A nutrition programme should be adopted and integrated into comprehensive intervention programmes to target iron-deficiency anaemia among female adolescents in Palestine.
OBJECTIVE: In this study, we aim to investigate the involvement of heme oxygenase-1 (HO-1) in the anti-inflammatory effects of ZnC in lipopolysaccharide (LPS)-induced RAW 264.7 murine macrophages.
MATERIALS AND METHODS: We used immunoblotting analysis to evaluate the involvement of HO-1 in the anti-inflammatory effects of ZnC and the signaling pathway involved was measured using Dual luciferase reporter assay.
RESULTS: Results from immunoblotting analysis demonstrated that pretreatment of cells with ZnC enhanced the expression of HO-1 in RAW 264.7 cells. Pretreatment of cells with HO-1 inhibitor (tin protoporphyrin IX dichloride) significantly attenuated the inhibitory effects of ZnC on nitric oxide (NO) production, inducible nitric oxide synthase (iNOS) expression and NF-κB activation in LPS-induced RAW 264.7 cells, suggesting that HO-1 play an important role in the suppression of inflammatory responses induced by ZnC. Furthermore, results from co-immunoprecipitation of Nrf2 and Keap1 and dual luciferase reporter assay showed that pretreatment of ZnC was able to activate the Nrf2 signaling pathway. Treatment of cells with p38 inhibitor (SB203580), c-Jun N-terminal kinase inhibitor (SP600125), and MEK 1/2 inhibitor (U0126) did not significantly suppress the induction of HO-1 by ZnC. Moreover, our present findings suggest that the effects of ZnC on NO production, HO-1 expression, and Nrf2 activation were attributed to its Zn subcomponent, but not l-carnosine.
CONCLUSION: Pretreatment with ZnC was able to activate Nrf2/HO-1 signaling pathway, thus suppressing the expression of inflammatory mediators, such as NO and iNOS in LPS-induced RAW 264.7 cells.
METHODS: Cell counting kit 8(CCK8), 5-ethynyl-2'-deoxyuridine (EdU), transwell and wound healing assays were conducted to study the influence of ZnC in the proliferating, invading and migrating processes of CRC cell lines (HCT116, LOVO) in vitro. The antitumor activity ZnC as well as its effects on tumor immune microenvironment were then assessed using CRC subcutaneous tumors in the C57BL/6 mouse model.
RESULTS: According to CCK8, EdU, transwell and wound healing assays, ZnC inhibited CRC cell lines in terms of proliferation, invasion and migration. ZnC could inhibit miR-570 for up-regulating PD-L1 expression. In vivo experiments showed that gavage (100 mg/kg, once every day) of ZnC inhibited the tumor growth of CRC, and the combination of ZnC and anti-PD1 therapy significantly improved the efficacy exhibited by anti-PD1 in treating CRC. In addition, mass cytometry results showed that immunosuppressive cells including regulatory T cells (tregs), bone marrow-derived suppressor cells (MDSC), and M2 macrophages decreased whereas CD8+ T cells elevated after adding ZnC.
CONCLUSIONS: The present study reveals that ZnC slows the progression of CRC by inhibiting CRC cells in terms of proliferation, invasion and migration, meanwhile up-regulating PD-L1 expression via inhibiting miR-570. The ZnC-anti-PD1 co-treatment assists in synergically increasing anti-tumor efficacy in CRC therapy.
METHODS: This study is part of the Long-term Research Grant Scheme - Towards Useful Ageing cohort study in Malaysia. Of a total of 174 participants with complete trace elements and oxidative and DNA damage data during baseline, only 147 (84.5%) were successfully followed up after 18 months. Participants who experienced any fall events in the previous 18 months during the follow-up were categorized as fallers.
RESULTS: Thirty participants (20.4%) reported at least one fall in the previous 18 months. The mean concentrations of aluminium, lead and zinc were significantly higher (P
METHODS: The TCGA portal was employed in this investigation to find APOC1 expression in CRC. Its correlation with other genes and clinicopathological data was examined using the UALCAN database. To validate APOC1's cellular location, the Human Protein was employed. In order to forecast the relationship between APOC1 expression and prognosis in CRC patients, the Kaplan-Meier plotter database was used. TISIDB was also employed to evaluate the connection between immune responses and APOC1 expression in CRC. The interactions of APOC1 with other proteins were predicted using STRING. In order to understand the factors that contribute to liver metastasis from CRC, single-cell RNA sequencing (scRNA-seq) was done on one patient who had the disease. This procedure included sampling preoperative blood and the main colorectal cancer tissues, surrounding colorectal cancer normal tissues, liver metastatic cancer tissues, and normal liver tissues. Finally, an in vitro knockdown method was used to assess how APOC1 expression in tumor-associated macrophages (TAMs) affected CRC cancer cell growth and migration.
RESULTS: When compared to paracancerous tissues, APOC1 expression was considerably higher in CRC tissues. The clinicopathological stage and the prognosis of CRC patients had a positive correlation with APOC1 upregulation and a negative correlation, respectively. APOC1 proteins are mostly found in cell cytosols where they may interact with APOE, RAB42, and TREM2. APOC1 was also discovered to have a substantial relationship with immunoinhibitors (CD274, IDO1, and IL10) and immunostimulators (PVR, CD86, and ICOS). According to the results of scRNA-seq, we found that TAMs of CRC tissues had considerably more APOC1 than other cell groups. The proliferation and migration of CRC cells were impeded in vitro by APOC1 knockdown in TAMs.
CONCLUSION: Based on scRNA-seq research, the current study shows that APOC1 was overexpressed in TAMs from CRC tissues. By inhibiting APOC1 in TAMs, CRC progression was reduced in vitro, offering a new tactic and giving CRC patients fresh hope.
DESIGN: The study was conducted using the quantitative descriptive method with a cross-sectional design. Data were collected using an FFQ and sociodemographic, sedentary behaviour and physical activity questionnaires. Anthropometric measurements and blood analyses were also conducted.
SETTING: The study population included all Palestinian female adolescents enrolled in secondary schools in the academic years 2015-2016. Five female secondary schools were selected randomly from five governorates of the Gaza Strip.
SUBJECTS: Female adolescents (n 330) aged 15-19 years in the selected secondary schools were enrolled randomly.
RESULTS: Prevalence of anaemia, ID and IDA among female adolescents in the Gaza Strip, Palestine, was 35·8, 40·3 and 26·0 %, respectively. A significant association (P<0·05) existed between ID, anaemia and IDA and dietary habits, including skipping breakfast and amount of junk food intake. Also, low consumption of fruits and vegetables was associated with IDA in the female adolescents. A statistically significant association was found between mother's education and ID but not with the other sociodemographic factors.
CONCLUSIONS: The study shows that there is an alarming problem of anaemia and IDA in the Gaza Strip, Palestine. This may indicate that there are insufficient nutrition education programmes, particularly inside schools or by the mass media.