Obesity is demonstrated to be a risk factor in the development of cancers of various organs, such as colon, prostate, pancreas and so on. Leptine (LEP) is the most renowned of the adipokines. As a hormone, it mediates its effect through leptin receptor (LEPR), which is widely expressed in various tissues including colon mucosa. In this study, we have investigated the degree of expression of LEP and LEPR in colorectal cancer (CRC). We collected 44 surgically resected colon cancer tissues along with normal adjacent colon tissue (NACT) from a sample of CRC patients from the Malaysian population and looked for leptin and leptin receptors using immunohistochemistry (IHC). All the samples showed low presence of both LEP and LEPR in NACT, while both LEP and LEPR were present at high intensity in the cancerous tissues with 100% and 97.7% prevalence, respectively. Both were sparsed in the cytoplasm and were concentrated beneath the cell membrane. However, we did not find any significant correlation between their expression and pathological parameters like grade, tumor size, and lymph node involvement. Our study further emphasizes the possible causal role of LEP and LEPR with CRC, and also the prospect of using LEPR as a possible therapeutic target.

Background Studies suggest excessive screen time (use of smartphones, televisions, computers and/or video games) is linked to speech and language delay. This study explored the sociodemographic characteristics of children with speech delay in Kuantan, Malaysia, and the association of screen time with speech and other developmental delays. Methods This cross‐sectional study was conducted between July and November 2019 at the child psychiatry and speech therapy clinics, at Kuantan Hospital, Pahang, Malaysia. Parents of children with speech delay aged <72 months provided information on their children's and their own screen times. Speech and other developmental skills were assessed using the Schedule of Growing Skills II with scores reported as developmental quotient (DQ) level. Results The study included 91 children (67 boys, 24 girls) of whom 54.9% had primary speech delay and 45.1% had neurodevelopmental disorders; their mean age was 39.9 ± 11.52 months. The children's mean screen time was 2.26 ± 1.98 h daily, with 36.3% exceeding 2 h. Higher children's screen time was moderately correlated with higher parental screen time (rs = 0.479, P < 0.01). Household income was positively correlated with screen times of the children and the parents (rs = 0.243, P = 0.02 and rs = 0.390, p < 0.01, respectively). Parents who intended to reduce their children's screen time reported higher screen time in their children (t(89) = 2.322, P = 0.023). Children's age was positively correlated with the number of types of screen media (rs = 0.225, P = 0.032). The mean speech DQ was 54.76 ± 24.06%. Lower speech DQ was associated with lower DQs in other skills (P < 0.01). No significant correlation was shown between children's and parents' screen time with DQs of speech and other skills (P > 0.05). Conclusion The correlation between parent and child screen time provides an opportunity for possible intervention, where necessary. Larger studies are required to examine this correlation further.

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Objectives: To assess the role of leptin in human colonic adenocarcinoma and to establish its expression in Malay population patients by using immunohistochemistry study. Methodology: Immunohistochemical study (IHC) using antibodies against leptin and its receptor was applied to assess the expression of leptin and its receptor in 38 samples of adenocarcinoma of the colon among Malay population and compare this expression with that of the adjacent normal colon tissue. Results: All the 38 colon adenocarcinoma samples stained strongly (100%) for leptin and 36 out of 38 also stained strongly for leptin receptor (95%). The other 2 (5%) stained weak (1+). However, the whole specimens of the normal adjacent colon tissue stained weakly (1+) for both leptin and leptin receptor. The expression of both hormones in cancer and normal tissue is significantly different (p<0.01). There was significant co-expression of both hormones in colonic cancerous tissue. Conclusions: Leptin/leptin receptor system may have a tumorigenic effect on the colon tissue, most likely by an autocrine process. Inhibition of leptin/leptin receptor system might be helpful in the prevention and management of colon cancer.

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