- Belal Hassanzadeh added an answer:4Does anyone have experience with stereology on testis paraffin sections?
We want to examine the effects of one chemotherapy medicine on mouse spermatogenesis and we need to compare the number of spermatids, spermatocytes, spermatogonia, Sertoli and Leydig cells between two groups. Can we use the paraffin sections for this purpose or we have to provide resin sections?
Thank you allFollowing
- Nguyen Xuan Phuoc added an answer:5Has anyone thought what factors or substances initiate oocyte release GDF9 ?
We know that GDF9 secrete from oocyte and affected to granulosa cells and may make it from flat cell to become cuboidal cell. And I wonder which is the factor or anything stimulate oocyte ?
thank you so much for all wonderful answer from you. It helps me a lot. In my opinion, I think I could be a substance from neuron or from vascular.Following
- Mark A Crowe added an answer:6What is the effect of GnRH on the estrous cycle in small ruminants?
Does the GnRH hormone have the same effect in small ruminants as in cows?
Specifically, what is its effect on ovulation, recruitment of follicular wave and synchronization of estrous cycle?
Yes and that is likely due to stage of follicle growth at the time of GnRH.Following
- Maria Bettencourt Pires added an answer:25What are the effects of contraceptives on their own target-organs, as on the Endometrium?
At the turn of the century, after more than 40 years of worldwide use of oral contraceptives, the international scientific community is still researching and learning new facts on the possible side effects of this surprisingly most prescribed hormonal medication. Peripheral and systemic vascular effects are a well-established fact. Astonishingly, not much has been established on the vascular effects of hormonal therapy directly on the main target-organ, the uterine and ovarian vasculature.
I am trying to build an update on this issue.
Would anyone please help me on this question? Thank you.
Thank you, dear Fatima. So, I feel happy if my long field of research produces some new knowledge...
When we work hard, we enjoy the feeling of being helpful.
Thank you for your comment.Following
- Sergio Torloni added an answer:1Would anybody have a protocol for leukocyte antibody detection?
This is a cross match test to determine the presence of anti- lymphocyte antibody in female partners suffering from immune mediated infertility, Like that developed by Dr Alan Beer and currently offered in his Lab and Rosalind Franklin Lab, Chicago. Would also be used in transplantation studies
I believe there are kits for this. The American Red Cross (ARC)Specialty lab does this, as well as NIH. These are micro well plates. These are serological tests. I would contact ARC in S. California (formerly Dr. Garratty's lab). Dr. Garraty passed last year. There they do flow cytometry crossmatches. They would be the first I would talk to.
Mixed lymphocyte studies is a pretty old method to do this, but it actually works well. This would be for cellular immunity.
Hope this helps
- Sawsan Talib added an answer:14Should we give 5000 or 10000 units of hCG to trigger ovulation?
Should we be using 5000 or 10000 IU hCG to trigger ovulation ?
if there is risk of OHSS so 5000 if not 10000 is better to induse ovulationFollowing
- Thomas W Kelsey added an answer:3Is there any evidence which shows prevalence of polycystic ovary syndrome reduced by increasing gravidity?
Does PCOS rate declined in women after the first parturition?
How this subject can be explained?
There is good evidence that nulliparity is more common in PCOS (see Mikola M, Hiilesmaa V, Halttunen M, Suhonen L, Tiitinen A. Obstetric outcome in women with polycystic ovarian syndrome. Hum Reprod. 2001;16:226–229.) Hence, indirectly, it could be plausibly argued that increased gravidity is associated with decreased PCOS. This seems to be the wrong way round, though. PCOS (the condition) should increase or decrease a measurable related outcome (parity/gravidity), rather than your stated question.Following
- Mohammad Mosarof Hossain added an answer:7Would scientists can go for any alternatives to producemMonosex tilapia (Oreochromis niloticus) other than 17 methyl testosterone hormone?
For the commercial production of Monosex tilapia (Oreochromis niloticus) all male 17 methyl testostrone hormones are widely used in many parts of the Globe including Bangladesh. Though it might be rumor or not but is further claimed as the causative agents to infertility, moustache and appearing unusual hairs in different organs of women.
Would scientists can assists me concerning the matter and would we go for any alternatives to produce Monosex (Oreochromis niloticus) other than 17 methyl testostrone hormone?
Dear Ndakalimwe Naftal Gabriel,
Sorry for late to sharing with you regarding the incorporation of electric field / electrode/ electro-magnetic field to separate the male and female zygote during breeding of Tilapia. Dear Please visit the following link to find more about the matter.
- Filippo Mancuso added an answer:9What is role of GnRH-2?
What is physiological role of GnRH-2 in humans?
According to Yen & Jaffe's Reproductive Endocrinology is still unknown.
GnRH-2 regulates reproduction in females by stimulating the secretion of both luteinizing- and follicle-stimulating hormonesFollowing
- Louis Macovsky added an answer:1What kind of estrogen-androgen balance is all about?
It is interesting to know, the authors well know about of the biology of the human fetus? Physiology of human pregnancy is that between the fetus and the mother's body, there is a organ that up to 24 perform of the function of the endocrine system of the fetus, that is the placenta. This is the first thing. Secondly to maintain a normal pregnancy need huge concentration of estrogen and progesterone, but androgens are not, the content of which is negligible (if at all they circulate in the blood of the fetus) during pregnancy. That is why the male fetus in contrast to in the female fetuses for at least of the period of fetal development and several years after spermatogenesis is not occurs, as it requires at least a minimum amount of androgens. That's why when any threats abortion obstetricians artificially increases the concentration of estrogens and progestins in pregnant women to prevent miscarriage. Third, start the production of hormones in fetus begins only at 20-24 weeks of development, after maturation of the pituitary gland, which is coincident with the first of brain potentials. And at the end, placenta - a powerful factor in hormone metabolism and almost all steroids and androgens generally transformed by aromatase necessary to maintain pregnancy in estrogens. Therefore, the big question is level of which hormones increases by congenital adrenal hyperplasia of fetus? What kind of estrogen-androgen balance is all about? But hypotheses is the hypotheses, whatever it was.
From FETAL AND NEONATAL PHYSIOLOGY Volume 2 PN 9996076415 FOURTH EDITION 2011, p. 319: (hopefully this helps)
Gonadal sex steroids exert an important influence on the pubertal growth spurt, but absence of these factors is not noticeable in prepubertal growth.197 But even in early life, gonadal and adrenal sex steroids in excess can cause a sharp increase in growth rate as well as the premature appearance and progression of secondary sexual features. Sex steroids exert a direct effect on long bone growth, mainly through conversion to estrogen, and can increase GH secretion, once GH receptors are present in adequate supply. Untreated virilizing congenital adrenal hyperplasia is compatible with survival, sometimes for years, as long as severe hypoglycemia or shock does not develop; in those children who have achieved such a state of stability, growth acceleration may occur early in infancy; if the adrenopathy also is of the salt-losing type, the failure to thrive will mask any tendency toward increased growth rate, and the child will grow poorly until treatment is supplied or the child dies from hyponatremia, hyperkalemia, and hypoglycemic shock. Familial Leydig and germinal cell maturation may also cause increased growth early in the first year. If unabated, increased sex steroids will cause advancement of skeletal age, premature epiphyseal fusion, and short adult stature. Thus, just as growth deceleration requires evaluation, growth acceleration can be just as abnormal and may be a sign of precocious puberty or virilizing congenital adrenal hyperplasiaFollowing
- Christopher R Harlow added an answer:5Can anyone suggest a RBC lysis buffer recipe?
Dear all, I am working with bovine granulosa cells. Recently, I have moved to a new lab and I lost my previous protocol to prepare RBC lysis buffer which is suitable for granulosa cells collected for culturing. If anyone have a RBC lysis buffer recipe which is suitable for granulosa cells, please let me know.
Thanks in advance for your time.
I have 2 suggestions that I have used for human and rodent granulosa cells.
1. Gravity sedimentation and repeated dilution with PBS. Add a large volume of PBS (around 30ml to the sample in a 60ml Falcon tube. Leave to stand for 5 minutes. The more dense granulosa cells will sink to the bottom of the tube. Carefully aspirate most of the supernatant and then repeat 2 or 3 times. This will get rid of most of the RBCs.
2. Pellet the sample by centrifugation at 200-300g. Add 10 ml sterile water, mix rapidly (5-10 seconds) , then quickly add an equal volume of a 2x strength cell culture medium (available from Gibco) to restore the osmotic balance.. The RBCs are very sensitive to the hypo-osmotic shock and will rupture.
I hope this helps
- S.V. Krishna Reddy added an answer:6Does anybody have any evidence or have used Cabergoline in idiopathic male factor infertility?
prolactin level is normal
In females clinical presentation like anovulation, amenorrhea, galactorrhea is earlier even in small microadenoma but in male prolactinoma requires large in size to cause clinical symptoms due to pressure effects & loss of libido and oligospermia in11% of males due to secondary hypogonadism. Hence dopamine agonists can is useful in female as these can regress the tumour but since the tumour is large in male medical followed by surgical treatment may be necessary.
Pratiba singh et al.Hyperprolactinemia: An often missing cause of male infertility. Journal of Human Reproductive sciences- vol 4,issue 2, may-aug-2011:102-103.
Dhole GR. et al - EUA Guidelines on male infertility- Eur Urol 2005;48:703-11Following
- Kulvinder kochar kaur added an answer:3Are polycystic ovaries relevant for PCOS?
Well, they give the name to the syndrome – but are they really central to the clinical presentation? The current definition allows a patient to have PCOS without the presence of PCO. Affected patients suffer from hyperandrogenism – hirsutism, acne and alopecia – which is linked to hyperandrogenemia: Is there solid data to support the notion that patients with PCO more often have hyperandrogenism or are more severely affected? PCOS also presents with a- or oligomenorrhea – which is linked to anovulation and thus reduced fertility. Wedge resection of the ovaries or other techniques to reduce the number of cysts = follicles like ovarian drilling improves fertility – does that mean the reduction of “cysts” is the cure or is this rather a stimulant in itself or the result of the concomitant reduction of androgens? Also, PCO does not influence the metabolic consequences of PCOS, such as insulin resistance, glucose intolerance or obesity. Apparently, PCOS may even be defined without PCO, as the 1990 NIH definition did – or was this merely an expression of lesser emphasis on ultrasound in the USA than in Europe? What does the inclusion of PCO in the 2003 Rotterdam definition improve, other than widening the spectrum of patients, some of which do not even have a relevant clinical problem (e.g. PCO plus hyperandrogenemia without hyperandrogenism)? How do we really define PCO: The number of “cysts” per ovary to separate “true” PCO from healthy women with multiple follicles has increased from 10 to 12, and recently to over 25  – how is that practical in routine work? Earlier  and recent work  suggests that PCO morphology does not associate with significant consequences for health in the absence of other symptoms of PCOS – why then should we bother and why should we not opt for a better name for the syndrome?
 Dewailly D et al. Definition and significance of polycystic ovarian morphology: a task force report from the Androgen Excess and Polycystic Ovary Syndrome Society. Human Reproduction Update 20:334–352, 2014
 Legro RS et al. Polycystic Ovaries Are Common in Women with Hyperandrogenic Chronic Anovulation but Do Not Predict Metabolic or Reproductive Phenotype. J Clin Endocrinol Metab 90: 2571–2579, 2005
i think i already mentioned about ruling out 21 hyderoxylase deficiency has to be ruled out before diagnosing PCOS AND ONE CAN PUT A PATIENT AS PCOS only if patient satsfies one of the 2 criterias laid down by ricardo azziz s modified in 2009 and he has eplained in detail how to rule out all 21 hydroxylase deficiency as well as CRF stimulation tests but problem is if none of these criteria are fulfilled then one doesnt have to investifgate even for 21 hydroxylase as one can find simple polycystic ovaries in normal women without anty evidece of hyperandrogensm or irregular cycles eg hirsutism etc .Another point to be highlighted is allcases of PCOS are not due to hyperinsulinemia and a blanket putting of metformin is not justified without testing for insulin resistance and routine diane tjerapy which occurs as per dictation of pharmacy reps should be stopped as some amount of androgen is required as a precursor for normal steroidogenesis in folliculogenesis and it oes a lot of harm by suppressing testosterone markedly by such prolonged cyproterone in combination with ee.Following
- Elanor N Wainwright added an answer:3Do you know mouse mutant lines where homozygous female are healthy but sterile due to the absence of germ cells?
We are looking for mouse females that do have normal ovaries but do not have germ cells (no oocytes). I know that some of the different Sl or W alleles that can give that phenotype but I would like to know if there are others mutant lines.
You could use busulfan-treatment to deplete germ cells or stop-floxed DTA line crossed with specific germ cell creFollowing
- Gerado Martín Oresti added an answer:9Is it possible to isolate germ cells (pachytene or pre- pachytene stage) from mice testis for in vitro culture?I want to isolate and culture germ cells of pachytene or pre-pachytene stage from mice testis to study my drug effect, but i can't find any precise protocol to do so. Is it possible to culture germ cells without a feeder layer of somatic cells?
Yes, you can use STAPUT with excelent resultsFollowing
- Ali Saeed Al-Chalabi added an answer:1Does anyone have a protocol for Testicular marker enzyme assays particularly for ALP, SDH, LDH and ACP) in mice?
I would just like to make a request for the protocols for screening Testicular marker enzyme assays( ALP, SDH, LDH and ACP) in mice.
I tried to hard to find one but couldn't. In some studies enzyme assay kits have been used, which seems to be very expensive.
I also wanted the protocol for estimating harmonal levels(Testosterone). But even for this I could see kits for assaying.
Please can anyone let me know if there is a protocol I can follow.
pleased find the attached pdf and link
- Tom Adejoh added an answer:11Is anyone interested in poly-cystic ovary syndrome induction without chemical or hormone therapy?We designed a chemical induction free animal model (in rat) for PCOS and are designing projects for better evaluation of brain physiologic characteristic of this disease. We will be glad for other researcher collaboration on this subject.
I am a Radiographer with competence in sonography and Computed Tomography. If you are interested in the use of these modalities to evaluate your specimens, then count me in. Thank you.Following
- D. Erickson added an answer:1Does somebody know of a book about comparative mice-human physiology?I need a book about reproductive mice physiology, and better if its compared to the human one. I'm working in research about the hormonal effects in cancer development in mice model and need some backup about it and the similarities to the human model.Following
- Petra Roosen added an answer:1Does anyone know of a provider of the hormone used for sex reassignment surgery: 17 alpha methyltestosterone?I'm from Peru and I need to buy (import) this product as soon as possible.
Maybe you mistook the name of the desired hormone? For a male to female hormonal (not: surgical) reassignment it is 17β-Estradiol. If this is what you are researching, ask your doctor to prescribe it. The medication itself is comparably cheap in its generic form and available world-wide.Following
- CHEBOUB Amina added an answer:2Is aromatisation the only source of estrogen in adult male?I want to know if the inhibition of aromatase is a total inhibition of the production of estrogen?Thank you very muchFollowing
- Vicki Clifton added an answer:1How does the level of dihydrotestosterone in blood vary before, during, and after ejaculation in human males?If not known in humans, what about in other mammals? Please feel free to direct me to literature sources.Manfred Schedlowski has published work on hormone profile of men and women before, during and after masturbation and sexual intercourseFollowing
- Weronika Rupik added an answer:2Is there anyone with experience in neonatal mice ovaries ablation?I want to collect newborn (1 day) mice ovaries to study it microscopically, but I can't find precise/complete information about the procedure.Hi Daniel, please, write what kind of microscopic examination you plan (electron, light or immuno).Following
- Veena Vidyasagar asked a question:OpenWhat are the causes of menstrual disturbances in hypothyroidism?Abnormal uterine bleeding and hypothyroidismFollowing
- Matthew James Conroy added an answer:1Real time PCR primers for oestrogen and progesterone gene in pigs?I want to study the real time expression of oestrogen and progesterone gene in pigs (RIA being not possible in my case). Whenever I do a nucleotide search in NCBI it gives me back only the results for receptors of both the genes. Since these two hormones being tissue specific, I want to study the gene itself and not receptors. Does anyone have any articles/references/suggestions in this regard ?You will not find a gene for either of these hormones, because steroid hormones are not gene products.Following
- Manjeet Kaur Sharma added an answer:7I am looking for a methods or any drug administrable to rats, in order to induce sexual arousal. Does anything exist?I was wondering if sexual arousal in one rat can induce sexual stimulation in other one, separated from each other, kept in different cages about 2 meter from each other.As a postdoc I was working with a PhD student who was trying to study feedback effects of DHT on FSH. She was injecting DHT to rats over a period of several days to induce infertilty. But when we mated the treated males with naive females, it increased their fertility status because we saw a spurt in the number of pups! At the time I was new to the field and did not know that in rats T/DHT actually induce the release of pituitary FSH! Higher androgens would also increase mating behaviour.
Look up this publication:Studies on the effects of low doses of 5 alpha-dihydrotestosterone (DHT) on the basal levels of serum gonadotropins and the sensitivity of the pituitary to luteinizing hormone releasing hormone (LHRH) in adult male rats.Karanth S, Gill MK, Dutta A, Juneja HS. Hormone and Metabolic Research 01/1984; 16(1):32-36.
Also try and look up the t for an approprite publication on the behavioural effects of estrogen on male sexual behaviour/mounting.Male rats mate with proestrus females very early in the morning which can be checked either from plugs/sperm in vaginal smears/diestrus from 10-20 days.Following