Identification of the Variations in the CPT1B and CHKB Genes Along with the HLA-DQB1*06:02 Allele in Turkish Narcolepsy Patients and Healthy Persons

The pretrial process of discovery governed by Federal and Maine Rule of Civil Procedure 26 enables plaintiffs in product liability actions to delve where few people have delved before—into a corporation\u27s internal memoranda, competitive practices, and secret product or design information as well as other less sensitive information in a company\u27s possession. Discovery, in this context as in others, is a powerful tool determined by the courts to be necessary for the just litigation of claims. As a balance to the leeway given parties to compel production of information in discovery, federal and Maine courts have the authority under Federal and Maine Rule 26(c) to protect parties and witnesses from the harm that can result from a disclosure of confidential information. The court may enter a protective order, sometimes called a confidentiality order, restricting a party receiving the information from disseminating it or from making any use of the information other than for purposes of the specific litigation. In addition, public access to information after its use in the litigation often is barred by such orders. Irrespective of the legal interests of the parties involved in the case, however, the public outside the legal community may have an interest in the information, and the receiving party may wish to disclose it. This point is brought into focus by the occasional case in which confidential information raises dramatic health issues, such as the recent reports of potential health risks from silicone breast implants. Judicial use of Rule 26(c) to restrict dissemination of discovered information predictably has invited First Amendment claims of free speech. Maine courts are empowered and exhorted by Maine Rule 26(c) to issue protective orders. Unlike the Federal Rule, Maine Rule 26(c) includes an admonition for the courts to exercise their powers to grant a protective order and other controls over discovery “with liberality . . . to protect parties and witnesses.” Whether conscious of the admonition or not, state courts in product liability cases have issued broadly constructed protective orders restricting plaintiffs, their attorneys and their witnesses from revealing information. The risk for all trial courts, confronted with the potential magnitude of discovery problems and hesitant to spend their limited time on this one procedural issue, is that the power to grant protective orders will degenerate into a perfunctory granting of most or even all such requests. The decision to grant such an order becomes perfunctory when the court does so without an appropriate “good cause” determination and without a careful fashioning of the order to minimize its impact on the affected parties. In Maine\u27s courts, despite the admonition to use the protective-order power liberally, the same considerations apply as fully as in federal courts to a determination of whether a protective order is justified. This Comment examines these considerations and concludes that trial courts must guard against exercising too freely their power to issue protective orders. Such an overly broad exercise of the power relieves movants of their burden to articulate with some specificity the potential harm constituting good cause for restricting parties\u27 and witnesses\u27 First Amendment interests. An understanding of the implications of protective orders should encourage courts to fashion such orders in a way that minimizes the effect on the parties and witnesses without sacrificing the protective purpose of the order

Identification of the Variations in the CPT1B

Background: The HLA-DQB1*06:02 allele across all ethnic groups and the rs5770917 variation between CPT1B and CHKB genes in Japanese and Koreans are common genetic susceptibility factors for narcolepsy. This comprehensive genetic study sought to assess variations in CHKB and CPT1B susceptibility genes and HLA-DQB1*06:02 allele status in Turkish patients with narcolepsy and healthy persons. Methods: CHKB/CPT1B genes were sequenced in patients with narcolepsy (n=37) and healthy persons (n=100) to detect variations. The HLA-DQB1*06:02 allele status was determined by sequence specific polymerase chain reaction. Results: The HLA-DQB1*06:02 allele was significantly more frequent in narcoleptic patients than in healthy persons (p=2×10(−7)) and in patients with narcolepsy and cataplexy than in those without (p=0.018). The mean of the multiple sleep latency test, sleep-onset rapid eye movement periods, and frequency of sleep paralysis significantly differed in the HLA-DQB1*06:02–positive patients. rs5770917, rs5770911, rs2269381, and rs2269382 were detected together as a haplotype in three patients and 11 healthy persons. In addition to this haplotype, the indel variation (rs144647670) was detected in the 5′ upstream region of the human CHKB gene in the patients and healthy persons carrying four variants together. Conclusion: This study identified a novel haplotype consisting of the indel variation, which had not been detected in previous studies in Japanese and Korean populations, and observed four single-nucleotide polymorphisms in CHKB/CPT1B. The study confirmed the association of the HLA-DQB1*06:02 allele with narcolepsy and cataplexy susceptibility. The findings suggest that the presence of HLA-DQB1*06:02 may be a predictor of cataplexy in narcoleptic patients and could therefore be used as an additional diagnostic marker alongside hypocretin