Was immer Menschen interessiert, schlägt sich in Büchern und Bildern nieder. So sind Portraitgemälde typisch für die bürgerliche europäische Kunst seit der Renaissance; sie führen uns ein gewandeltes Selbstbild vor Augen. In Leipzig kann man nun Affen-Portraits studieren.

Although human biomedical and physiological information is readily available, such information for great apes is limited. We analyzed clinical chemical biomarkers in serum samples from 277 wild- and captive-born great apes and from 312 healthy human volunteers as well as from 20 rhesus macaques. For each individual, we determined a maximum of 33 markers of heart, liver, kidney, thyroid and pancreas function, hemoglobin and lipid metabolism and one marker of inflammation. We identified biomarkers that show differences between humans and the great apes in their average level or activity. Using the rhesus macaques as an outgroup, we identified human-specific differences in the levels of bilirubin, cholinesterase and lactate dehydrogenase, and bonobo-specific differences in the level of apolipoprotein A-I. For the remaining twenty-nine biomarkers there was no evidence for lineage-specific differences. In fact, we find that many biomarkers show differences between individuals of the same species in different environments. Of the four lineagespecific biomarkers, only bilirubin showed no differences between wild- and captive-born great apes. We show that the major factor explaining the human-specific difference in bilirubin levels may be genetic. There are human-specific changes in the sequence of the promoter and the protein-coding sequence of uridine diphosphoglucuronosyltransferase 1 (UGT1A1), the enzyme that transforms bilirubin and toxic plant compounds into water-soluble, excretable metabolites. Experimental evidence that UGT1A1 is down-regulated in the human liver suggests that changes in the promoter may be responsible for the human-specific increase in bilirubin. We speculate that since cooking reduces toxic plant compounds, consumption of cooked foods, which is specific to humans, may have resulted in relaxed constraint on UGT1A1 which has in turn led to higher serum levels of bilirubin in humans.

Individuals endowed with a ‘Theory of Mind’ (‘ToM’) understand themselves and others as agents whose actions are driven by unobservabl e psychological states. How and when human infants come to such an understa nding has been extensively resear ched in the visual domain. In my dissertation, I addressed three gaps in the extant literature about what great apes’ know about others' visual perceptions and perceptual beliefs. In study 1, I investigated orangutans’ understanding of visual attenti on and others’ visual perspectives in a competitive situation. Overall, the results suggest that orangutans have a limited understanding of others’ perspectives, relying mainly on cues from facial and bodily orientation and egocentric ruleswhen making perspective judgements. In study 2, I explored whether apes and 20 month old human infants requesting a desired object from a human experimenter would use communicative means to direct visual attention towards the object. While infants used pointing to alter the experimenter’s focus of attention, we found no evidence that apes’ employ their point gestures in this way. In study 3, I examined chimpanzees’ and 5.5 year old human children’s understanding of perceptual beliefs. By designing two novel false belief tasks which required reduced executive functioning, I attempted to find out whether chimpanzees’ historical failure in explicit false belief tasks was due to their lack of inhibitory control Neither the chimpanzees nor the 5.5 year-olds succeeded in the novel tasks.

Although human biomedical and physiological information is readily available, such information for great apes is limited. We analyzed clinical chemical biomarkers in serum samples from 277 wild- and captive-born great apes and from 312 healthy human volunteers as well as from 20 rhesus macaques. For each individual, we determined a maximum of 33 markers of heart, liver, kidney, thyroid and pancreas function, hemoglobin and lipid metabolism and one marker of inflammation. We identified biomarkers that show differences between humans and the great apes in their average level or activity. Using the rhesus macaques as an outgroup, we identified human-specific differences in the levels of bilirubin, cholinesterase and lactate dehydrogenase, and bonobo-specific differences in the level of apolipoprotein A-I. For the remaining twenty-nine biomarkers there was no evidence for lineage-specific differences. In fact, we find that many biomarkers show differences between individuals of the same species in different environments. Of the four lineagespecific biomarkers, only bilirubin showed no differences between wild- and captive-born great apes. We show that the major factor explaining the human-specific difference in bilirubin levels may be genetic. There are human-specific changes in the sequence of the promoter and the protein-coding sequence of uridine diphosphoglucuronosyltransferase 1 (UGT1A1), the enzyme that transforms bilirubin and toxic plant compounds into water-soluble, excretable metabolites. Experimental evidence that UGT1A1 is down-regulated in the human liver suggests that changes in the promoter may be responsible for the human-specific increase in bilirubin. We speculate that since cooking reduces toxic plant compounds, consumption of cooked foods, which is specific to humans, may have resulted in relaxed constraint on UGT1A1 which has in turn led to higher serum levels of bilirubin in humans.