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Social views regarding masturbation taboo have varied greatly in different cultures, and over history. Various medical and psychological benefits have been attributed to a healthy attitude toward sexual activity in general and to masturbation in particular. No causal relationship is known between masturbation and any form of mental or physical disorder.[7][8] Masturbation is considered by clinicians to be a healthy, normal part of sexual enjoyment. As epidemiological studies of pain typically rely on self-report via surveys or telephone interviews, one potential problem can be nonparticipation bias114,224; that is, differences in the outcome of interest between persons willing to participate and those that decline to do so.432 The higher the participation rate, the less bias will be introduced. Some studies report participation rates, and fewer test for differences between participants and nonparticipants as often little information is available from nonparticipants.

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Moreover, the inconsistency of findings from brain imaging studies can be attributed not only to the vast methodological differences across studies but also to their small sample sizes. Sex differences in endogenous pain modulation have received more limited attention, but the available evidence suggests that males and females may differ in this regard as well, though the direction and magnitude of the effects are quite variable. The mechanisms and practical importance of these sex differences merit further investigation in future studies.

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In the next step, two additional carbon atoms are removed by the CYP17A1 (17α-hydroxylase/17,20-lyase) enzyme in the endoplasmic reticulum to yield a variety of C19 steroids.[157] In addition, the 3β-hydroxyl group is oxidized by 3β-hydroxysteroid dehydrogenase to produce androstenedione. In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone. Because testicular differentiation occurs without SRY in approximately 20% of individuals with 46,XX testicular DSD, there might be other important genes that cause 46,XX testicular DSD19). SOX9 on chromosome 17q24.3 is one of the genes that plays an important role in the development of the skeleton and genital organs4).

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• Abundant evidence from recent epidemiologic studies clearly demonstrates that women are at substantially greater risk for many clinical pain conditions, and there is some suggestion that postoperative and procedural pain may be more severe among women than men.
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Suffering the ridicule of his colleagues, he abandoned his work on the mechanisms and effects of androgens in human beings. However, the results of a recent study suggested that duplication of SOX9 is not a common cause of 46,XX testicular or 46,XX ovotesticular DSD8). In that study, the authors amplified microsatellite markers in the region of SOX9 from a cohort of 30 patients with either 46,XX testicular or 46,XX ovotesticular DSD to detect SOX9 duplications, but they could not find any duplication of the SOX9 region in 17q. They implied that there might be another important cause of 46,XX testicular DSD8). Another gene, SOX3, has recently been identified as upregulating the expression of SOX9 via a similar mechanism to SRY and as being responsible for XX male sex reversal in humans through gain-of-function mutations mediated by genomic rearrangements around SOX3, possibly leading to its altered regulation10).

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