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Experimentations were carried out in aseptic rat model to extrapolate, according to the yardstick of rigorous basic science, the neurology of a specific portrayal of a VMAT2 on societally characterized peers in terms of tracing hepatic APR to life-threatening neural provocation. In other words, it is a basic trial to link psychologically-induced hepatic injury to organic repercussions; primarily heart maladies, diabetes, gastritis, kidney-liver failures, infertility, etc. Ultimately, to mimic the exposure of the dispossessed congregated in snubbed subdivides within a walking distance to downtown Cairo; e.g., Necropolis and Zabbalein ghettos, two rat models were tackled. The daily routine of aseptic rats was imperilled according to a combination of different schedules of availing chew and water together with a neurological injury emanating from exposure to recorded sound of cats in fierce fighting. USN and random feeding of rat model evoked a different APR format of neuro-inflammation whose levels of APR proteins attained maximal and minimal changes at the 3rdd, which did not regress to aseptic levels post > 15d of neurotic intoxication. That may suggest possible defensive biological-internalization of concomitant neurological and organic injuries but not necessarily healing. Similarly, DLSN showed a typical profile of APR with regression of APR proteins closer to aseptic levels. As expected, DLSN of diabetic rats displayed a steady decrease in serum’s free glucose together with concomitant increase in the relative concentrations of Ag, Hp, Fb and At while those of Alb and Pre-Al remained close to healthy levels. Rats’ provided with drinking water embracing DE-contaminants developed a range of mute APR on 3rd-6thd of intoxication while substantial liver cirrhosis was visualized on d15. DLSN of pathological rat models at points of maximal APR, e.g., (i) carrageenan-injured (1d), (ii) TAM-cirrhotic (100d)and (iii) DE-intoxicated (15d) rats, highlighted an unorthodox APR. For example, substantial -76%, -51, and -33% depletion of Alb, Ag, and Fb respectively while pre-albumin was not detectable on 15d of neurotically provoked DE model suggests substantial hepatic necrosis. Nonetheless, observed massive proteolysis of these serum proteins is deemed essential to provide intrahepatic cellular pool with monomeric carbohydrates and amino acids necessary for maintaining the remaining viable hepatocytes, however fatigued. These observations in rats’ model paralleled the diagnosis of a very low percentage of defensive APR reactants and cardiac maladies-induced early mortality (24-50y range) in the environmentally and mentally-intoxicated dispossessed Egyptians. Nonetheless, the modest increase in the concentrations of Hg and At on 3rdd and 7thd of neurotic provocation of DE model may be indicative of increased efficacy of intoxicated hepatocytes undergoing possible proliferation. It remains, psychosis of fear-induced hepatic APR is a hereditary protocol that is retained into the long-range memory of rats regardless of the milieu of breeding, e.g., aseptic laboratory conditions or filthy sewages’ milieu. Extrapolation of current data suggests humans may share certain distant evolutionary protocol(s) of neural behavioral patterns with early species, viz., de novo storage in giant marine snail Aplysia californica to reactions to noxious stimulation. Although too late, our conclusion is a modest one of the many warnings to the infiltration of de novo mental aberrations and drug-resistant second-generations of mutated organic diseases into the industrialized world. Issues presented here remain worthy of further experimentations and elaborations in the advanced world that is mercilessly caught in-between the grinding stones of the ancient and contemporary mills, VMAT2 and scientific adventures of hexose polyester and GMOs respectively. Part II of our studies is pertaining to the relevance of bacterial and/ or enzymatic precipitation of organic maladies, e.g., malignancies, cardiovascular diseases, male ineptness, gastritis and kidney failures. Statistically, it is not a coincidence these injuries are 2-3 times rampant among the dispossessed dwelling in the filthy quarters of the city. Results involving deranged lipid distribution, bacterial pods and extraction of microplastics found in tissue of harvested fish from the heavily polluted River Nile and the Alexandrian shoreline will be published in Part III. Correspondence to: Cyril Baradaeus, The Samaritan Biochemists, 279 Khaled ben Walied, Seidi Gaber, Alexandria, Egypt, E-mail: bioscience001@yahoo.com Received: October 02, 2017; Accepted: October 21, 2017; Published: October 24, 2017 Abbreviations: VMAT2: Vesicular monoamine transporter 2; MAOA: Monoamine Oxidase A; APR: Acute-phase response; DLSN: Day Light Scheduled Neurosis; USN: Unscheduled Neurosis; 2D-IEP: 2-dimension immunoelectrophoresis; HCV4b: Hepatitis C 4b; HBP: Helicobacter pylori; CHD: Cardiac heart diseases; RO: Reverse osmosis; TAM: Thioacetamide; DE: Diesel exhaust; HPE: Hexose polyester; GMO: Genetically modified organism; Necropolis: City of the dead; Zabbalein: Rubbish Collectors; Alb: Albumin; pre-Alb: Pre-albumin, Hp: Haptoglobin; At: α-1-antitrypsin; Fb: Fibrinogen; Ag: α-1acidglycoprotein

The dispossessed of Egypt, Part I: Anatomy of hepatic-APR to environmental filth and VMAT2’s variant-induced psychosis in aseptic rat models