The population history of the indigenous populations in island Southeast Asia is generally accepted to have been shaped by two major migrations: the ancient "Out of Africa" migration ∼50,000 years before present (YBP) and the relatively recent "Out of Taiwan" expansion of Austronesian agriculturalists approximately 5,000 YBP. The Negritos are believed to have originated from the ancient migration, whereas the majority of island Southeast Asians are associated with the Austronesian expansion. We determined 86 mitochondrial DNA (mtDNA) complete genome sequences in four indigenous Malaysian populations, together with a reanalysis of published autosomal single-nucleotide polymorphism (SNP) data of Southeast Asians to test the plausibility and impact of those migration models. The three Austronesian groups (Bidayuh, Selatar, and Temuan) showed high frequencies of mtDNA haplogroups, which originated from the Asian mainland ∼30,000-10,000 YBP, but low frequencies of "Out of Taiwan" markers. Principal component analysis and phylogenetic analysis using autosomal SNP data indicate a dichotomy between continental and island Austronesian groups. We argue that both the mtDNA and autosomal data suggest an "Early Train" migration originating from Indochina or South China around the late-Pleistocene to early-Holocene period, which predates, but may not necessarily exclude, the Austronesian expansion.

Bis[benzyl N'-(indol-3-ylmethylene)-hydraz inecarbodithioatoJ-nickel(lI) (BIHCN) has been used in traditional medicine for their biological activities. The present study was performed to evaluate the anti ulcerogenic activity of BIHCN against ethanol induced gastric mucosal injury in rats. Six groups of adult Sprague Dawley rats were orally pre-treated respectively with 10% Tween 20 solution (ulcer control group), omeprazole 20 mg/kg (reference group), and 50,100,200 and 400 mg/kg of BIHCN in 10% Tween 20 solution (experimental groups) one hour before oral administration of absolute ethanol to generate gastric mucosal injury. After an additional hour, the rats were sacrificed and the ulcer areas of the gastric walls were determined. Grossly, the ulcer control group exhibited severe mucosal injury, whereas pre-treatment with compound exhibited significant protection of gastric mucosal injury. Histological studies of the gastric wall revealed that ulcer control group exhibited severe damage of gastric mucosa; along with edema and leucocytes infiltration of submucosal layer compared to rats pre-treated with BIHCN which showed comparatively gastric mucosal protection, reduction or absence of edema and leucocytes infiltration of submucosal layer. Acute toxicity study of BIHCN with a higher dose of 5 g/kg did not manifest any toxicological signs in rats. In conclusions, the present finding suggests that BIHCN promotes ulcer protection as ascertained grossly by significant reduction of ulcer area, and histologically by comparatively decreases in ulcer areas, reduction or absence of edema and leucocytes infiltration of submucosal layer compared to ulcer control group. ulcer. period of addition of carbon disulfide. To the mixture, 40% ethanol (60 m]) was added and the solution was cooled in ice. Benzyl chloride (25.3 g, 0.2 mol) was then added slowly with vigorous stirring. The white product was separated by filtration, washed with water and dried in air. The crude product was recrystallized from absolute ethanol; yield, 23 g (58%).

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Ethanol extracts of different traditional Malaysian plants (Polygonum minus, Andrographis paniculata, Curcuma xanthorrhiza,Momordica charantia and Strobilanthes crispus) were evaluated for their gastroprotective activities. In this experiment several groups of Sprague Dawley rats weighing 200–250gm were used. The first group was pre treated with (0.25% w/v) carboxymethyl cellulose (negative control, 5 ml/kg), the second group was pre treated with 20 mg/kg omeprazole (positive control) and the other groups were pretreated with the selected Malaysian medicinal plants in two different doses 250 and 500 mg/kg respectively. After 60 min all the rats were treated with 95% ethanol for ulcer induction. Rats were sacrificed 1 h after induction and the stomachs were analyzed for gross and histological changes. Negative control group showed extensive lesions of gastric mucosal layer, whereas rats pretreated with omeprazole and Malaysian plants showed significant and dose dependent reduction in gastric lesions. Amongst, the selected plants Polygonum minuspotentially promote better inhibition percentage of ulcer area. So that we can conclude that Polygonum minus could be the selective plant as an antiulcerogenic agent for the treatment of gastric ulcer.

Indolic compounds have attracted a lot of attention due to their interesting biological properties. The present study was performed to evaluate the subacute toxicity and anti-ulcer activity of BClHC against ethanol-induced gastric ulcers. Experimental animal groups were orally pre-treated with different doses of BClHC (50, 100, 200 and 400 mg/kg) in 10% Tween 20 solution (vehicle). Blank and ulcer control groups were pre-treated with vehicle. The positive group was orally pretreated with 20 mg/kg omeprazole. After one hour, all groups received absolute ethanol (5 mL/kg) to generate gastric mucosal injury except the blank control group which was administered the vehicle solution. After an additional hour, all rats were sacrificed, and the ulcer areas of the gastric walls determined. Grossly, the ulcer control group exhibited severe mucosal injury, whereas pre-treatment with either derivative or omeprazole resulted in significant protection of gastric mucosal injury. Flattening of gastric mucosal folds was also observed in rats pretreated with BClHC. Histological studies of the gastric wall of ulcer control group revealed severe damage of gastric mucosa, along with edema and leucocytes infiltration of the submucosal layer compared to rats pre-treated with either BClHC or omeprazole where there were marked gastric protection along with reduction or absence of edema and leucocytes infiltration of the submucosal layer. Subacute toxicity study with a higher dose of derivative (5 g/kg) did not manifest any toxicological signs in rats. In conclusions, the present finding suggests that benzyl N'-(5-chloroindol-3-ylmethylidene)hydrazinecarbodithioate promotes ulcer protection as ascertained by the comparative decreases in ulcer areas, reduction of edema and leucocytes infiltration of the submucosal layer.