A reviewer of a book I wrote claimed an idea presented therein could be found elsewhere. Nine years later, no one could say where, but no one would correct the erroneous claim, so what be-gan as an effort to obtain a redress of a legitimate grievance slowly degenerated into a tour d’farce of a surreal ethics warp in our intellectual community. The citations submitted to docu-ment the claim failed to do so, and the file on the dispute maintained by the American Psychological Association (APA) really is not about my case at all. The University of Connecticut (UConn) and the American Association for the Advancement of Sci-ence (AAAS) failed to hold anyone accountable. There was a basic conflict between the conduct of officials of all these organiza-tions and their ethical codes. In a culture of intellectual cor-ruption, behavior consisted of a pervasive and extended cover-up characterized by sophistry, secrecy, fantasy, irrelevance, ra-tionalization, misattribution, misrepresentation, fabrication, falsification, failure to communicate and an adamant refusal to deal logically and fairly with the facts of the case. This demon-strated a complete lack of cognitive integrity and constituted a total betrayal of the academic/scientific commitment to truth.

Acute ischemic stroke has been recognized as one key cause of vascular cognitive impairment (VCI). The purpose of this study was to evaluate the correlation between carotid artery stenosis and post VCI in acute ischemic stroke patients.

Decompressive craniectomy is widely used for treating patients with traumatic brain injury (TBI). Usually patients have dura mater defect due to surgery or injury itself. The defective area may left open or repaired by artificial dura substitutes. A variety of artificial dura substitutes have been used for this purpose.

Fatigue is a common and disabling problem in patients with Parkinsons disease (PD), and there is currently no satisfactory treatment. As acupuncture has been reported to be effective in fatigue related to other conditions, we sought to evaluate its efficacy in PD.

Symptoms of DHMN2 usually begin from the age of 10 to the middle of adulthood. Early signs of this disorder include clogging or weakness in the muscles of the toe and the next, the whole leg. The DHMN2 syndrome is caused by the mutation of the HSPB1 gene, which is positioned in the long arm of chromosome 7 as 7q11.23, and the HSPB8 gene, which is based on the long arm of chromosome 12, is 12q24.23.