METHODOLOGY: Twenty-four children referred consecutively to the University of Malaya Medical Centre who fulfilled Apley's criteria (at least three episodes of abdominal pain severe enough to affect normal activity over a period longer than 3 months) were tested for lactase deficiency using a pocket breath test analyser (BreatH2 meter; Europa Scientific, Cheshire, England). Lactulose was used to check for hydrogen-producing capacity.
RESULTS: There were 14 males and 10 females in the study, consisting of five Malays, 14 Chinese and five Indians. Mean age was 9.9 years. Seventeen of the 24 children (70.8%) with recurrent abdominal pain who underwent the breath hydrogen test had a positive result. In those with a negative result, subsequent lactulose administration resulted in a positive rise in breath hydrogen. None of the 24 children developed abdominal pain during the test. All the Indian subjects, 71.4% of the Chinese subjects and 40% of the Malay subjects with recurrent abdominal pain had lactase deficiency. The proportion of boys and girls with lactase deficiency was similar (71.4 vs 70.0%, respectively). There was no significant difference between lactase sufficient and deficient children with recurrent abdominal pain with regard to sex, age, ethnic group and clinical features. Following a lactose-free diet, none of the children in the breath hydrogen positive and negative groups reported any appreciable difference in pain symptoms.
CONCLUSIONS: The prevalence of lactase deficiency among this group of Malaysian children with recurrent abdominal pain was high, but lactase deficiency did not appear to play an important role in causing the symptoms.
Methods: Lactase activity was measured with a 13CO2 lactose breath test using an infrared spectrometer. Each subject took 25 g of lactose naturally enriched in 13CO2 together with 250 mL of water after an overnight fast. Breath samples were collected at baseline and at 15-min intervals for 180 min. Subjects were asked to report gastrointestinal (GI) symptoms following ingestion of the lactose test meal.
Results: Of the 248 subjects tested, 216 (87.1%) were lactase deficient. We found no significant differences in the presentation of LD between gender and races. LD was found in 87.5% of males and 86.8% of females (P = 0.975) and in different races: Chinese (88.5%) versus Malay (83.1%) (P = 0.399), Indian (90.5%) versus Malay (P = 0.295), and Chinese versus Indian (P = 0.902). LI was diagnosed in only 49 (19.8%) subjects; 35 patients had diarrhea, while the remainder had at least two other GI symptoms after the lactose meal.
Conclusion: The prevalence of LD was high in all three major ethnic groups-Malays, Chinese, and Indians. Ironically, the prevalence of LI was low overall.
Methods: Myoblast cells were cultured into young and senescent state before treated with different concentrations of ginger standardised extracts containing different concentrations of 6-gingerol and 6-shogaol. Analysis on cellular morphology and myogenic purity was carried out besides determination of SA-β-galactosidase expression and cell cycle profile. Myoblast differentiation was quantitated by determining the fusion index, maturation index, and myotube size.
Results: Treatment with ginger extracts resulted in improvement of cellular morphology of senescent myoblasts which resembled the morphology of young myoblasts. Our results also showed that ginger treatment caused a significant reduction in SA-β-galactosidase expression on senescent myoblasts indicating prevention of cellular senescence, while cell cycle analysis showed a significant increase in the percentage of cells in the G0/G1 phase and reduction in the S-phase cells. Increased myoblast regenerative capacity was observed as shown by the increased number of nuclei per myotube, fusion index, and maturation index.
Conclusions: Ginger extracts exerted their potency in promoting muscle regeneration as indicated by prevention of cellular senescence and promotion of myoblast regenerative capacity.