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The control of human reproduction

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The control of human reproduction

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    3. Menstrual cycle lengths

    4. Menstruation is an external indicator of ovarian events controlled by the hypothalamic-pituitary axis OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based. This synchronisation is between many parts of the body.. Ovary, uterus, oviduct, brain, vagina. And is achieved by hormones! - very dynamic Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things: a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization) b) time for response - eg. E2 induces mitoses cornification in vagina at oestrus AFTER peak of e2 c) profile that matters - interactions between P and e (e.g. implantation window) In rats, pattern of T and androstenedione mirror e2 Dominant progestin is 20 alpha OH-P - from newly formed CL OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based. This synchronisation is between many parts of the body.. Ovary, uterus, oviduct, brain, vagina. And is achieved by hormones! - very dynamic Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things: a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization) b) time for response - eg. E2 induces mitoses cornification in vagina at oestrus AFTER peak of e2 c) profile that matters - interactions between P and e (e.g. implantation window) In rats, pattern of T and androstenedione mirror e2 Dominant progestin is 20 alpha OH-P - from newly formed CL

    9. Where do follicles come from?

    11.

    12. Why do some follicle die and not others? Model for agieing in other systemsWhy do some follicle die and not others? Model for agieing in other systems

    13. The life history of a follicle?

    15. Oestradiol is the major steroid secreted by the follicle

    17. In sheep, follicular development takes 180 daysIn sheep, follicular development takes 180 days

    18. In sheep, follicular development takes 180 daysIn sheep, follicular development takes 180 days

    26. OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based. This synchronisation is between many parts of the body.. Ovary, uterus, oviduct, brain, vagina. And is achieved by hormones! - very dynamic Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things: a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization) b) time for response - eg. E2 induces mitoses cornification in vagina at oestrus AFTER peak of e2 c) profile that matters - interactions between P and e (e.g. implantation window) In rats, pattern of T and androstenedione mirror e2 Dominant progestin is 20 alpha OH-P - from newly formed CL OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based. This synchronisation is between many parts of the body.. Ovary, uterus, oviduct, brain, vagina. And is achieved by hormones! - very dynamic Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things: a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization) b) time for response - eg. E2 induces mitoses cornification in vagina at oestrus AFTER peak of e2 c) profile that matters - interactions between P and e (e.g. implantation window) In rats, pattern of T and androstenedione mirror e2 Dominant progestin is 20 alpha OH-P - from newly formed CL

    27. OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based. This synchronisation is between many parts of the body.. Ovary, uterus, oviduct, brain, vagina. And is achieved by hormones! - very dynamic Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things: a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization) b) time for response - eg. E2 induces mitoses cornification in vagina at oestrus AFTER peak of e2 c) profile that matters - interactions between P and e (e.g. implantation window) In rats, pattern of T and androstenedione mirror e2 Dominant progestin is 20 alpha OH-P - from newly formed CL OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based. This synchronisation is between many parts of the body.. Ovary, uterus, oviduct, brain, vagina. And is achieved by hormones! - very dynamic Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things: a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization) b) time for response - eg. E2 induces mitoses cornification in vagina at oestrus AFTER peak of e2 c) profile that matters - interactions between P and e (e.g. implantation window) In rats, pattern of T and androstenedione mirror e2 Dominant progestin is 20 alpha OH-P - from newly formed CL

    35. OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based. This synchronisation is between many parts of the body.. Ovary, uterus, oviduct, brain, vagina. And is achieved by hormones! - very dynamic Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things: a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization) b) time for response - eg. E2 induces mitoses cornification in vagina at oestrus AFTER peak of e2 c) profile that matters - interactions between P and e (e.g. implantation window) In rats, pattern of T and androstenedione mirror e2 Dominant progestin is 20 alpha OH-P - from newly formed CL OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based. This synchronisation is between many parts of the body.. Ovary, uterus, oviduct, brain, vagina. And is achieved by hormones! - very dynamic Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things: a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization) b) time for response - eg. E2 induces mitoses cornification in vagina at oestrus AFTER peak of e2 c) profile that matters - interactions between P and e (e.g. implantation window) In rats, pattern of T and androstenedione mirror e2 Dominant progestin is 20 alpha OH-P - from newly formed CL

    36. OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based. This synchronisation is between many parts of the body.. Ovary, uterus, oviduct, brain, vagina. And is achieved by hormones! - very dynamic Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things: a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization) b) time for response - eg. E2 induces mitoses cornification in vagina at oestrus AFTER peak of e2 c) profile that matters - interactions between P and e (e.g. implantation window) In rats, pattern of T and androstenedione mirror e2 Dominant progestin is 20 alpha OH-P - from newly formed CL OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based. This synchronisation is between many parts of the body.. Ovary, uterus, oviduct, brain, vagina. And is achieved by hormones! - very dynamic Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things: a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization) b) time for response - eg. E2 induces mitoses cornification in vagina at oestrus AFTER peak of e2 c) profile that matters - interactions between P and e (e.g. implantation window) In rats, pattern of T and androstenedione mirror e2 Dominant progestin is 20 alpha OH-P - from newly formed CL

    37. OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based. This synchronisation is between many parts of the body.. Ovary, uterus, oviduct, brain, vagina. And is achieved by hormones! - very dynamic Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things: a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization) b) time for response - eg. E2 induces mitoses cornification in vagina at oestrus AFTER peak of e2 c) profile that matters - interactions between P and e (e.g. implantation window) In rats, pattern of T and androstenedione mirror e2 Dominant progestin is 20 alpha OH-P - from newly formed CL OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based. This synchronisation is between many parts of the body.. Ovary, uterus, oviduct, brain, vagina. And is achieved by hormones! - very dynamic Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things: a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization) b) time for response - eg. E2 induces mitoses cornification in vagina at oestrus AFTER peak of e2 c) profile that matters - interactions between P and e (e.g. implantation window) In rats, pattern of T and androstenedione mirror e2 Dominant progestin is 20 alpha OH-P - from newly formed CL

    39. Other changes in the cycle

    40. Uterine changes in the menstrual cycle.

    43. What causes the onset of menstruation?

    47. Cervical mucus

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