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The pectoralis major muscle forms the base of the breast, which extends from the second to sixth rib early in life but may extend to below the sixth rib as the breast matures and sags. The breast is anchored to the pectoralis major fascia by the Cooper ligaments. However, these ligaments are flexible and allow for movements in the breast. In most women, the Cooper ligaments become stretched with time and age, eventually resulting in a ptotic breast. Because of gravity, the lower pole of the breast is fuller than the upper pole. At the lateral edges of the breast, the tail of Spence extends in the axilla.
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Breast development or mastogenesis starts around the sixth week of gestation. The milk line, which is a distinct linear elevation, appears around the seventh week. At the end of the eighth week, the rudimentary breast forms from the thickened white line and will eventually become the mature breast. Throughout embryogenesis, there is a proliferation of basal cells. At about 30 weeks of gestation, occlusion of the papillary bag results in the formation of the nipple areolar complex. The final nipple will appear at about 38 to 40 weeks.
The breasts of an adult woman are milk-producing, tear-shaped glands. They are supported by and attached to the front of the chest wall on either side of the breast bone or sternum by ligaments. They rest on the major chest muscle, the pectoralis major.
The mature breast is located within the anterior thoracic wall, lying atop the pectoralis major muscle. Pubertal changes lead to incomplete development of the breast , a process which is only completed during pregnancy . The incomplete breast consists mostly of adipose tissue but also lactiferous units called lobes. These eventually drain into the lactiferous ducts and then into the lactiferous sinus and then to the nipple-areolar complex. During pregnancy , the breast undergoes both anatomic and physiologic changes to prepare for lactation. During the first trimester, the ductal system expands and branches out into the adipose tissue in response to the increase of estrogen. Elevated levels of estrogen also cause a decrease in adipose tissue and ductal proliferation and elongation. Estrogen also stimulates the pituitary gland which leads to elevated levels of prolactin. By the twentieth week of gestation, mammary glands are sufficiently developed to produce components of milk due to prolactin stimulation. Milk production is inhibited by high estrogen and progesterone levels and colostrum is produced during this time. In the third trimester and then rapidly after birth, these levels decrease, allowing for milk production and eventual let-down to allow for breastfeeding. Most pregnancies cause the areola to darken, the breast to increase in size, and the Montgomery glands to become more prominent. Post-lactational involution occurs at the cessation of milk production caused by a decline in prolactin.
Of the two common implant placement options, submuscular implants (implants that are placed under the breast muscle) are less obstructive during mammograms than subglandular implants (implants placed under the breast tissue but above the muscle).
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In people with muscular dystrophy, the broken genes are the ones that make the proteins that keep muscles healthy and strong. For example, those with Duchenne or Becker muscular dystrophies make too little of a protein called dystrophin, which strengthens muscles and protects them from injury.
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Muscle dysmorphia is a specific form of BDD. It can cause you to have negative feelings about your build and the appearance of your muscles (either for your entire body or one or more specific places on your body).
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Human artery smooth muscle cells (HASMCs) were used in this study. Glucose concentrations at 5 and 25 mM were defined as normal and HG status, respectively. The results showed that HG could increase the NLRP3, cleaved caspase 1, and pro/mature IL-1[beta] levels to induce the expressions of bone-related matrix proteins and subsequent HASMC calcification. This process was regulated by Akt activation and reactive oxygen species (ROS) production. Moreover, 6-shogaol could inhibit the Akt/ROS signaling and NLRP3/caspase 1/IL-1[beta] inflammasome and hence attenuated HASMC calcification.
Vascular calcification is highly prevalent for the patients with diabetes and chronic renal diseases and contributes to the further increased morbidity and mortality of cardiovascular complications. Although the therapeutic strategy for reducing blood glucose level has been extensively investigated, the vascular calcification development in diabetes patients have still remained [1-5]. Vascular calcification pathogenesis is a complex process with a phenotypic switch of vascular smooth muscle cells (VSMCs) to osteoblast- or chondrocyte-like cells, which initiates the upregulation and deposition of calcium phosphate and mineralization-related proteins, including osteopontin (OPN), osteocalcin (OCN), and alkaline phosphatase (ALP), in calcification regions and hence results in the stiffening of vessel walls [6-8]. Moreover, the signaling related to the bone/cartilage growth, including the bone morphogenetic proteins, Akt signaling, and runx2 transcription activity, has also been associated with the occurrence of vascular calcification complication of diabetes [8-12]. Currently, the precise mechanisms about how high blood glucose affects the vascular calcification pathogenesis in diabetes patients has not been completely elucidated. Therefore, more detailed investigation and understanding is still urgent and necessary for further improving the development of diabetes and its vascular calcification complications.
Vascular calcification derived from atherosclerosis and diabetes has been demonstrated to be a chronic inflammation event, which is regulated by inflammatory cytokines such as tumor necrosis factor (TNF)-[alpha] and interleukin (IL)-1[beta]. Therefore, inflammasome system has recently been implicated in the pathogenesis of vascular calcification [13-15]. NLRP3 complex, which is composed of NLRP3 protein, adaptor protein ASC, and caspase 1, has been indicated as one of important inflammasomes because of its regulatory role in autoimmune and inflammation [16-18]. After receiving the stimulations, intracellular NLRP3 level upregulation and subsequent caspase 1 activation could cleave the pro-IL-1[beta] and pro-IL-18 into mature and active IL-1[beta] and IL-18 and then consequently elicit inflammatory responses and diseases development [16-18]. Accumulating data has indicated that inflammasomes, including NLRP3 complex, are the important regulatory systems for the development of chronic metabolic diseases. In this study, we further examine whether high concentration of glucose, mimics the hyperglycemia environment of diabetes patients, stimulates vascular calcification through the NLRP3 inflammasome system.
In this study, we investigated the role of NLRP3 inflammasome in vascular calcification in response to high glucose environment and the possible antagonized role of 6-shogaol in this process. We found that NLRP3, cleaved caspase 1, and pro/mature IL-1[beta] proteins could be upregulated to initiate human artery SMC (HASMC) calcification under high concentration of glucose stimulation. Moreover, this NLRP3 inflammasome upregulation was resulted from the Akt activation and ROS production. Furthermore, we also demonstrated the antagonized role of 6-shogaol in NLRP3 inflammasome activation and subsequent HASMC calcification. Our findings provide new insights into the understanding of NLRP3 inflammasome-initiated HASMC calcification under high glucose stimulation and indicate a potential pharmaceutic role of 6-shogaol in cardiovascular complication of diabetes. 041b061a72