Ask Our Doctors – Archive
Our Medical Directors are outstanding physicians that you will find to be very personable and compassionate, who take care to ensure that you have the most cutting-edge fertility treatments at your disposal. This is your outlet to ask your questions to the doctors.
Hi good sir,
I am 40.5 years old, AMA 1.7 and FSH 7. I have h/o RPL of recent, all spontaneously conceived in last 2 years at age 38-40: 17 weeks (euploid female), 12 weeks (euploid female) and x 2 biochemicals. I have 3 earthside children also spontaneously conceived in my mid 30s. We’ve decided to do IVF for PGT-A (give my AMA) and concomitantly undergo reproductive immunology work up as well due to my RPL (I’ve been extensively worked up thus far by local academic REI; no balanced translocations in myself or husband, no autoimmune phenomena, possible thrombophilia risk with homozygosity for MTHFR A1298c).
I am not performing very well s/p x 2 retrievals spaced 1 mo apart am I’m confused why given that I’ve demonstrated I am quite capable of spontaneously conceiving without assistance thus far in life, including with my recent 12 week loss. First cycle I was on provera x 30 days after which stimulation protocol was commenced with lupron 10 u, gonal-f 200, and menopur 75. I stim’d for 9 days; retrieved 8 mature follicles, all 8 mature oocytes fertilized with ICSI, day 3 all rated fair to good (6-10 cells), but yielded only 3 blasts by day 6 (5CC x 2 which were discarded per lab protocol and a 5BB that was high level mosaic 12+). Second retrieval a few days ago went terrible. I started provera 6 days after my 1st retrieval (we are doing back to back retrievals) for 10 days, and then lupron was started 4 days after the start of provera as an overlap during priming phase at 10 u daily. 5 days after lupron 10 u was commenced, I was told to stop provera, continue lupron but half dose at 5 u and also to start my gonadatropins (gonal-f 200 and menopur 75). I stim’d for 9 days, but only retrieved 6 follicles, x4 M2 oocyctes, x1 M1 oocyte, and another oocyte that disintegrated. Day 3 report delivered today is dismal: only one that is rated good at 9 cell stage; the rest are 4 cells or less and rated poor.
What are we doing wrong? Why am I performing so terribly? No known sperm factor issues either. Also on usual recommended supplements but not on DHEA. Any insight on your end in terms of my protocols? Are some people just BAD at IVF and do better with in vivo fertilization such as IUI or natural? I’m admittedly surprised by my performance. And becoming increasingly despondent. Thank you sir!
Hello Dr. Sher,
What are your thoughts on platelet rich plasma (PRP) Is it something you would recommend for RPL?
Hi Dr Sher,
What are your thoughts on ERA testing?
If I am taking Progesterone the month before the ERA test does this distort the results? Should you be on a natural cycle the month before testing?
Thanks so much for all your help and support!
The blastocyst and the endometrium are in a constant state of cross-talk. In order for successful implantation to take place, the blastocyst must be at the appropriate stage of development, and needs to signal a well synchronized endometrium to ‘accept it”. This dialogue between embryo and endometrium involves growth factors, cytokines, immunologic accommodations, cell adhesion molecules, and transcription factors. These are all mostly genetically driven but are also heavily influenced by numerous physiologic, pathophysiologic, hormonal and molecular mechanisms capable of profoundly affecting the receptivity of the secretory endometrium to the overtures made by the embryo, to implant.
Embryo implantation takes place 6-9 days after ovulation. This period is commonly referred to as the “window of implantation (WOI)”. In the past it was believed that as long as the embryo reached the uterus in this 4 day time frame, its chance of implanting would not be affected.
In 2013, after evaluating 238 genes in the secretory endometrium and applying bioformatics, Ruiz-Alonzo, et all introduced the Endometrial Receptivity Array (ERA) . Using this test, they categorized mid-secretory endometria into 4 categories: “a) proliferative, b) pre-receptive, c) receptive or d) post-receptive”. They claimed that women with pre-receptive or post-receptive endometria were more likely to experience failed implantation post-embryo transfer (ET).
It was in large part this research which suggested that the concept of a relatively “wide” (4day) WOI, was flawed, that an optimal WOI is likely much narrower and could be a critical factor in determining the success or failure of implantation post-ET. Ruiz-Alonzo also reported that about 25% of women with recurrent IVF failure (RIF), have pre, or post-receptive endometria. They presented data suggesting that viable IVF pregnancy rates could be enhanced,
by deferring FET by about 24 hours in women who had pre-receptive endometria and bringing ET forward by the same amount of time, in women with post-receptive endometria,
There is no doubt that ERA testing has opened the door to an intriguing arena for research. Presently however, available data is inconclusive. Here, following recent studies are 2 dissenting opinions regarding the value for ERA:
•Basil and Casper (2018) state: “Performing the ERA test in a mock cycle prior to a FET does not seem to improve the ongoing pregnancy rate in good prognosis patients. Further large prospective studies are needed to elucidate the role of ERA testing in both good prognosis patients and in patients with recurrent implantation failure”
•Churchill and Comstock (2017) conclude:” In our preliminary observations, the non-receptive ERA group had similar live birth rates compared to the receptive ERA group. It appears the majority of the pregnancies conceived in the non-receptive group occurred during ovulatory cycles and thus a non-receptive ERA in a medicated cycle likely does not have prognostic value for ovulatory cycles. Larger studies are needed to assess the prognostic value of ERA testing in the gen-eral infertility population.”
There are additional negatives that relate to the considerable emotional and financial cost of doing ERA testing:
1.First, the process costs $600-$1000 to undertake
2., Second, it requires that the patient undergo egg retrieval, vitrify (cryobank) all blastocysts, res for 1 or more cycles to allow their hormonal equilibrium to restore, do an ERA biopsy to determine the synchronicity of the endometrium, wait a few weeks for the results of the test and thereupon engage in undertaking an additional natural or hormonal preparation cycle for timed FET. This represents a significant time lapse, emotional cost and additional expense.
Presently, ERA testing is only advocated for women who have experienced several IVF failures. However, some authorities are beginning to advocate that it become routine for women undergoing all IVF.
The additional financial cost inherent in the performance of the ERA test ($600-$1000), the considerable time delay in getting results, the fact that awaiting results of testing and preparing the patient for FET, of necessity extends the completion of the IVF/ET process by at least a few months, all serve to increase the emotional and financial hardship confronting patients undergoing ERA. Such considerations, coupled with the current absence of conclusive data that confirm efficacy, are arguments against the widespread use of ERA . In my opinion, ERA testing should presently be considered as being one additional diagnostic and be confined to women with “unexplained” RIF.
Gold standard statistical analyses require that all confounding variables be controlled while examining the effect of altering the one under assessment. There is an obvious interplay of numerous, ever changing variables involved in outcome following ET, e.g. embryo competency, anatomical configuration of the uterus and the contour of the endometrial cavity, endometrial thickness, immunologic and molecular factors as well as the very important effect of technical skill/expertise in performing the ET procedure …(to mention but a few). It follows that it is virtually impossible to draw reliable conclusions from IVF-related randomized controlled studies that use outcome as the end-point. This applies equally to results reported following “ gold standard” testing on the efficacy of ERA and, is one of the main reasons why I question the reliability of reported data (positive or negative).
The fact is that IVF (and related technologies) constitute neither a “pure science” nor a “pure art”. Rather they represent an “art-science blend”, where scientific principles applied to longitudinal experience and technical expertise coalesce to produce a biomedical product that will invariably differ (to a greater or lesser degree) from one set of clinical circumstances to another.
Since, the ultimate goal of applied Assisted Reproductive Medicine is to safely achieve the birth of a viable and healthy baby, the tools we apply, that are aimed at achieving this end-point, are honed through the adaptation of scientific principles and concepts, experience and expertise, examined and tested longitudinally over time. Needless to say, the entire IVF/ET process is of necessity subject to change and adaptation as new scientific and technical developments emerge.
This absolutely applies to the ERA as well!
Geoff Sher
PH: 702-533-2691
Hi Dr Sher,
I am currently trying naturally but take Progesterone after ovulation due to a luteal phase defect. Sometimes I have taken progesteron too long and start spotting whilst on it. I am now looking into doing an Era test prior to a medicated FET. Please could you advise if I should be on a natural cycle the cycle BEFORE doing the Era test (ie without progesterone in the luteal phase)? Will the progesterone from the cycle before distort the Era test results? As I have found my follicular phase seems to be shorter at times if I take the progesterone too long. Thanks so much!
I am not a believer in ERA testing. However, if you are resolved to go this route, then yes, it is wise to take a month off first. The progesterone used prior, should not affect the test!
Good luck!
Geoff Sher
My progesterone keeps dropping but my HCG keeps going up. My doctor has me on 200 mg of progesterone and now is moving me to 400mg of progesterone and will draw again in another week. Should I be concerned?
Round 1 of blood work :
HCG: 220
Progesterone: 8.8
Round 2:
HCG: 923
Round 3:
HCG: 4278
Progesterone: 5.8
Officially have a second failed cycle under our belt.
Two different protocols, 60 total eggs, 3 total blastocysts, 2 aneuploid (several abnormalities) and 1 euploid baby girl affected with my genetic condition.
At 27 & 28 years old we are pursuing IVF for what we thought were genetic reasons only. All of our fertility tests show normal, lifestyle is healthy, but embryo quality is apparently atrocious.
Our fertility clinic kind of made me feel like there wasn’t much else they could do to help me because my “stims cycles look great on paper.”
Hi Sydney,
You are clearly a rather high responder. In my opinion this means that you need a very individualized protocol for ovarian stimulation.
The importance of the IVF stimulation protocol on egg/embryo quality cannot be overstated. This factor seems often to be overlooked or discounted by t IVF practitioners who use a “one-size-fits-all” approach to ovarian stimulation. My experience is that the use of individualized/customized COS protocols can greatly improve IVF outcome. While no one can influence underlying genetics or turn back the clock on a woman’s age, any competent IVF specialist should be able to tailor the protocol for COS to meet the individual needs of the patient.
Gonadotropins (LH and FSH), whether produced by the pituitary gland or administered by way of fertility drugs, have different “targeted” sites of action in the ovary. FSH targets cells that line the inner wall of the follicle (granulosa cells) and also form the cumulus cells that bind the egg to the inner surface of the follicle. Granulosa cells are responsible for estrogen production.
LH, on the other hand, targets the ovarian connective tissue (stroma/theca) that surrounds ovarian follicles resulting in the production of male hormones such as testosterone (predominantly), androstenedione and DHEA. These androgens are then transported to the granulosa cells of the adjacent follicles in a “bucket brigade fashion”. There FSH converts testosterone to estradiol, causing granulosa cells to multiply (proliferate) and produce estradiol, follicles to grows and eggs to develop (ovogenesis) It follows that ovarian androgens (mainly testosterone) is absolutely indispensable to follicle/ egg growth and development.
However, the emphasis is on a “normal” amount of testosterone. Over-exposure of the follicle to testosterone can in my opinion, compromise egg development and lead to an increased likelihood of chromosomal irregularities (aneuploid) following LH/hCG-induced egg maturational division (meiosis) and compromise embryo “competency/quality.
Ovarian androgens can also reach the uterine lining where they sometimes will compromise estrogen receptor -induced endometrial growth and development.
A significant percentage of older women and those who have diminished ovarian reserve (DOR) have increased LH activity is increased. Such women either over-produce LH and/or the LH produced is far more biologically active. Chronically increased LH activity leads to overgrowth of ovarian connective tissue (stroma/theca). This condition, which is often referred to as Stromal Hyperplasia or hyperthecosis can result in excessive ovarian androgen/testosterone production and poorer egg-embryo quality/competency, Similarly, women with polycystic ovarian syndrome (PCOS), also characteristically have Stromal hyperplasia/hyperthecosis due to chronically increased LH activity. Thus they too often manifest with increased ovarian androgen production. It is therefore not surprising that “poor egg/embryo quality” is often also a feature of PCOS.
In my opinion, the over-administration of LH-containing menotropins such as Menopur, [which is comprised of roughly equal amount of FSH and hCG ,which acts similar to LH)], to older women, women with DOR and those who have PCOS can also lead to reduced egg/embryo competency . Similarly, drugs such as clomiphene or Letrozole that cause the pituitary gland to release excessive amounts of LH, are also potentially harmful to egg development and in my opinion, are best omitted from IVF COS protocols. This is especially the case when it comes to older women and those with DOR, who in my opinion should preferably be stimulated using FSH-dominant products such as Follistim, Puregon, Fostimon and Gonal-F.
Gonadotropin releasing hormone agonists (GnRHa): GnRHa such as Lupron, Buserelin, Superfact, Gonopeptyl etc. are often used to launch ovarian stimulation cycles. They act by causing an initial outpouring followed by a depletion of pituitary gonadotropins. This results in LH levels falling to low concentrations, within 4-7 days, thereby establishing a relatively “LH-free environment”. When GnRHa are administered for about 7 days prior to initiating gonadotropin stimulation (“long” pituitary down-regulation”), the LH depletion that will exist when COS is initiated, will usually be protective of subsequent egg development. In contrast, when the GnRHa administration commences along with the initiation of gonadotropin therapy, there will be a resultant immediate surge in the release of pituitary LH with the potential to increase ovarian testosterone to egg-compromising levels , from the outset of COS. This, in my opinion could be particularly harmful when undertaken in older women and those who have DOR.
GnRH-antagonists such as Ganirelix, Cetrotide and Orgalutron, on the other hand, act very rapidly (within hours) to block pituitary LH release. The purpose in using GnRH antagonists is to prevent the release of LH during COS. In contrast, the LH-lowering effect of GnRH agonists develops over a number of days.
GnRH antagonists are traditionally given, starting after 5th -7th day of gonadotropin stimulation. However, when this is done in older women and those (regardless of age) who have DOR, LH-suppression might be reached too late to prevent the deleterious effect of excessive ovarian androgen production on egg development in the early stage of ovarian stimulation. This is why, it is my preference to administer GnRH-antagonists, starting at the initiation of gonadotropin administration.
My preferred Protocols for Controlled Ovarian Stimulation (COS):
1.“Long” GnRHa (Lupron/Buserelin/Superfact/Gonopeptyl) Pituitary Down-regulation Protocol: The most commonly prescribed protocol for GnRHa/gonadotropin administration is the so-called “long protocol”. Here, GnRHa is given, starting a week or so prior to menstruation. This results in an initial rise in FSH and LH , which is rapidly followed by a precipitous fall to near zero. It is followed by a withdrawal bleed (menstruation), whereupon gonadotropin treatment should commence, while daily Lupron injections continue, to ensure a “low LH” environment. A modification to the “long protocol” which I prefer prescribing for older women and in cases of DOR, is the Agonist/Antagonist Conversion Protocol (A/ACP) where, upon the onset of a GnRHa-induced bleed, the agonist is supplanted by an antagonist (Ganirelix/Cetrotide/Orgalutron) and this is continued until the hCG trigger. In many such cases I often supplement with human growth hormone (HGH) in such cases in an attempt to enhance egg mitochondrial activity and so enhance egg development. This approach is often augmented with preimplantation genetic screening (PGS) of all embryos that reach the expanded blastocyst stage of development by day 5-6 post-fertilization. I also commonly recommend blastocyst banking to many such patients.
2.Short (“Flare”) GnRHa Protocol: Another GnRHa usage for COS is the so called “(micro) flare protocol”. This involves initiating gonadotropin therapy commensurate with initiation of gonadotropin administration. The supposed objective is to deliberately allow Lupron to elicit an initial surge (“flare”) in pituitary FSH release in order to augment FSH administration by increased FSH production. Unfortunately, this “spring board effect” constitutes “a double-edged sword”. While it indeed increases the release of FSH, it at the same time causes a surge in LH release. The latter can evoke excessive ovarian stromal/thecal androgen production which could potentially compromise egg quality, especially when it comes to older women and women with DOR. I am of the opinion that by evoking an exaggerated ovarian androgen response, such “(micro) flare protocols” can harm egg/embryo quality and reduce IVF success rates, especially when it comes to COS in older women, and in women with diminished ovarian reserve. Accordingly, I do not prescribe such protocols to my IVF patients.
3.Estrogen Priming – This is the approach I sometimes prescribe for my patients who have virtually depleted ovarian reserve , as determined by very low blood anti-Mullerian hormone AMH levels (<0.2ng/ml or 2 pmol/L) and are thus likely to be very “poor responders”. It involves a modified A/ACP. We start with estrogen skin patches applied every 2nd day (or with the BCP) for 10 days or longer, overlap it for 3 days with a GnRHa whereupon the estrogen priming is stopped. Th GnRHa is continued until the onset of menstruation (usually 5-7 days later) to cause pituitary LH, down-regulation. Upon menstruation and confirmation by ultrasound and measurement of blood estradiol levels that adequate ovarian suppression has been achieved, The patient is given twice-weekly injections of estradiol valerate (Delestrogen) for a period of 7-8 days whereupon COS is initiated using a relatively high dosage FSH-(Follistim, Fostimon, Puregon or Gonal F), which is continued along with daily administration of GnRH antagonist until the “hCG “trigger.” This approach is often augmented with HGH administration throughout the process of COS and by preimplantation genetic screening (PGS) of all embryos that reach the expanded blastocyst stage of development by day 5-6 post-fertilization. I also commonly recommend blastocyst banking to many such patients.
Estrogen Priming has succeeded in significantly enhancing ovarian response to gonadotropins in many of otherwise very poor responders.
Triggering egg Maturation prior to egg Retrieval: hCG versus GnRHa
With ovulation induction using fertility drugs, the administration of 10,000U hCGu (Pregnyl; Profasi, Novarel) or 500mcg hCGr (Ovidrel/Ovitrel) “trigger”) sends the eggs (into maturational division (meiosis). This process is designed to halve the chromosome number, resulting in mature eggs (M2) that will have 23 chromosomes rather that the 46 chromosomes they had prior to the “trigger”. Such a chromosomally numerically normal (euploid), mature (MII) eggs, upon being fertilized will (hopefully) propagate euploid embryos that have 46 chromosomes and will be “: competent” to propagate viable pregnancies. In my opinion, the key is to always “trigger” with no less than 10,000U of hCGu or 500mcg hCGr (Ovidrel/Ovitrel). Any lesser dosage often will reduce the efficiency of meiosis and increase the risk of the eggs being aneuploid. I personally do not use the agonist (Lupron) “trigger”, unless it is combined with (low dosage) hCG. The supposed reason for using the agonist, (Lupron) “trigger” is that by inducing meiosis through compelling a surge in the release of LH by the pituitary gland, the risk it reduces the risk of OHSS. This may be true, but it comes at the expense of egg quality because the extent of the induced LH surge varies and if too little LH is released, meiosis can be compromised, thereby increasing the likelihood of aneuploid and immature (MI) eggs. And there are other better approaches to preventing OHSS (e.g. “prolonged coasting”), in my opinion.
Use of the Birth Control Pill (BCP) to launch IVF-COS.
In natural (unstimulated) as well as in cycles stimulated with fertility drugs, the ability of follicles to properly respond to FSH stimulation is dependent on their having developed FSH-responsive receptors. Pre-antral follicles (PAF) do not have such primed FSH receptors and thus cannot respond properly to FSH stimulation with gonadotropins. The acquisition of FSH receptor responsivity requires that the pre-antral follicles be exposed to FSH, for a number of days (5-7) during which time they attain “FSH-responsivity” and are now known as antral follicles (AF). These AF’s are now able to respond properly to stimulation with administered FSH-gonadotropins. In regular menstrual cycles, the rising FSH output from the pituitary gland insures that PAFs convert tor AF’s. The BCP (as well as prolonged administration of estrogen/progesterone) suppresses FSH. This suppression needs to be countered by artificially causing blood FSH levels to rise in order to cause PAF to AF conversion prior to COS commencing, otherwise pre-antral-to –antral follicle conversion will not take place in an orderly fashion, the duration of ovarian stimulation will be prolonged and both follicle and egg development may be compromised. GnRH agonists cause an immediate surge in release of FSH by the pituitary gland thus causing conversion from PAF to SAF. This is why women who take a BCP to launch a cycle of COS need to have an overlap of the BCP with an agonist. By overlapping the BCP with an agonist for a few days prior to menstruation the early recruited follicles are able to complete their developmental drive to the AF stage and as such, be ready to respond appropriately to optimal ovarian stimulation. Using this approach, the timing of the initiation of the IVF treatment cycle can readily and safely be regulated and controlled by varying the length of time that the woman is on the BCP.
Since optimizing follicular response to COS requires that prior to stimulation with gonadotropins, FSH-induced conversion from PAF to AF’s first be completed and the BCP suppresses FSH, it follows when it comes to women launching COS coming off a BCP something needs to be done to cause a rise in FSH for 5-7 days prior to menstruation heralding the cycle of CO S. This is where overlapping the BCP with a GnRHa comes in. The agonist causes FSH to be released by the pituitary gland and if overlapped with the BCP for several days and this will (within 2-5 days) facilitate PAF to AF conversion…. in time to start COS with the onset of menstruation. Initiating ovarian stimulation in women taking a BCP, without doing this is suboptimal.
I strongly recommend that you visit www.SherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•The Fundamental Requirements For Achieving Optimal IVF Success
•Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
•Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
•Optimizing Response to Ovarian Stimulation in Women with Compromised Ovarian Response to Ovarian Stimulation: A Personal Approach.
•Egg Maturation in IVF: How Egg “Immaturity”, “Post-maturity” and “Dysmaturity” Influence IVF Outcome:
•Commonly Asked Question in IVF: “Why Did so Few of my Eggs Fertilize and, so Many Fail to Reach Blastocyst?”
•Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Staggered IVF
•Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation
•Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
•IVF: Selecting the Best Quality Embryos to Transfer
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
•PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
•IVF outcome: How Does Advancing Age and Diminished Ovarian Reserve (DOR) Affect Egg/Embryo “Competency” and How Should the Problem be addressed.
______________________________________________________
ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.
If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).
PLEASE SPREAD THE WORD ABOUT SFS!
Geoff Sher