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• The article concludes with a discussion of potential biopsychosocial mechanisms that may underlie sex differences in pain, and considerations for future research are discussed.
• Consistent with our previous reviews, current human findings regarding sex differences in experimental pain indicate greater pain sensitivity among females compared with males for most pain modalities, including more recently implemented clinically relevant pain models such as temporal summation of pain and intramuscular injection of algesic substances.
• A number of recent studies have tested for sex differences in chronic musculoskeletal pain at any site.
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You also can experience the thrill of anime AI chat free unblocked, and start free AI sex chat throuth ChatUp AI. Explore sexual characters, including an AI porn blonde girl and native American AI girl. The amount of testosterone synthesized is regulated by the hypothalamic–pituitary–testicular axis (Figure 2).[161] When testosterone levels are low, gonadotropin-releasing hormone (GnRH) is released by the hypothalamus, which in turn stimulates the pituitary gland to release FSH and LH. Finally, increasing levels of testosterone through a negative feedback loop act on the hypothalamus and pituitary to inhibit the release of GnRH and FSH/LH, respectively. The development of testes from bipotential gonadal primordia is controlled by complex molecular networks of expressions of multiple genes. Among the genes, SRY on the Y chromosome is a typical male-specific gene, which initiates testis development and directly upregulates the SRY-related HMG box-containing gene 9 (SOX9) gene expression.

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• The goal of this section is to examine whether more recent studies corroborate these findings.

More research is needed to further characterize the contribution of gender roles to the relationship between sex, gender, and pain. The results from 22 studies that examined sex differences in experimental heat pain are presented in the upper portion of Table 6. All of the studies used some form of contact heat with the exception of one study that used hot water immersion.360 Also, the forearm was the most common site for stimulus application. The vast majority of studies reported that females were more sensitive to heat pain than males. For the studies examining behavioral measures of heat pain sensitivity, 81% (12/17), and 94% (15/16) of the studies reported lower thresholds and tolerances, respectively, in females. Females were also found to rate heat pain as more intense and unpleasant in the majority of studies that included a suprathreshold protocol (7/9, 78%), and one study found that females required lower temperatures to evoke moderate pain.411 Overall, the hypothesis that heat pain sensitivity differs as a function of sex has been supported.

Here, we report a 4.2-year-old SRY-negative 46,XX boy with complete sex reversal caused by SOX9 duplication for the first time in Korea. He showed normal external and internal male genitalia except for small testes. Fluorescence in situ hybridization and polymerase chain reaction (PCR) analyses failed to detect the presence of SRY, and SOX9 intragenic mutation was not identified by direct sequencing analysis.

Haploinsufficiency of SOX9 from the loss of function mutations or deletions results in campomelic dysplasia (Online Mendelian Inheritance in Man #114290), which is a well-known skeletal dysplasia showing congenital bowing of long bones with male-to-female sex reversal in two-thirds of affected individuals with 46,XY20). On the other hand, duplication of SOX9 has been found in individuals with SRY-negative 46,XX testicular DSD. Previous studies have suggested that overexpression of SOX9 could induce testis determination in the absence of SRY4). In the present study, we also revealed SOX9 duplication as the cause of SRY-negative 46,XX testicular DSD by real-time PCR in a boy who presented with small testes and without any genital ambiguity. To our knowledge, this is the first report in Korea of 46,XX testicular DSD caused by SOX9 duplication.

A number of recent studies have tested for sex differences in chronic musculoskeletal pain at any site. In one study, women reported significantly higher ratings of worst and current pain intensity but there were no differences on the rating for least pain.351 We review evidence regarding several specific types of musculoskeletal pain, including back pain, widespread pain/fibromyalgia, and osteoarthritis. Research regarding sex and gender, differences in pain has increased substantially in recent years. As Fig 1 depicts, publications regarding sex, gender, and pain have increased at a much greater rate over the past 25 to 30 years relative to the pain field in general.

Surgery and other invasive procedures are accompanied by acute pain, and some surgical procedures confer substantial risk for the development of chronic pain.214 Several studies have reported on sex differences in acute pain following a variety of surgical procedures (see Table 4). Unfortunately, there is little standardization in the pain measures used or the time frame for assessing postoperative pain. There are no population level studies of postoperative pain; consequently, we review selected studies in clinical populations. LeResche243 reviewed several studies of temporomandibular joint pain that demonstrated a higher prevalence in women than men across the lifespan. Studies from Finland,322,352 Germany,159 Sweden,267 Turkey,309 the United States,326 Nigeria,302 and Brazil25 have drawn similar conclusions for tooth pain, jaw joint pain, and other orofacial pain conditions.

Sex hormones may influence multiple central nervous system pathways, including effects on the functioning of endogenous opioid systems, dopaminergic function, serotonergic activity, and other endogenous components involved in the nociceptive processing, as discussed below. Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (5α-DHT) by the cytoplasmic enzyme 5α-reductase. 5α-DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T.[147] The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA.