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Does Dehydroepiandrosterone (DHEA) improve in vitro fertilisation (IVF) outcomes in poor responders?

Malini MN, Zain MM

Med J Malaysia, 2020 01;75(1):24-28.
PMID: 32008015

BACKGROUND: In reproductive medicine poor ovarian response (POR) among women undergoing in vitro fertilisation (IVF) is of great concern. Meta-analysis showed that Dehydroepiandrosterone (DHEA) administration resulted in a significant increase in the number of oocytes retrieved in women with POR. The aim of this study was to assess the effectiveness of DHEA supplementation on IVF outcomes among poor responders undergoing IVF.
METHODS: Sixteen patients who were diagnosed with POR scheduled to undergo their second cycle of Intracytoplasmic sperm injection (ICSI)/embryo transfer cycle were enrolled. All enrolled patients had earlier undergone their first ICSI/embryo transfer cycle at least four months prior to this study. All subjects were given DHEA supplementation of 25mg three times daily for at least three months prior to their second ICSI/embryo transfer cycle. Statistical analysis of various ovarian response and ICSI outcomes parameter were compared pre and post DHEA.
RESULTS: Sixteen women with the mean age of 35 years were enrolled in the study. The comparative analysis of results showed a significant increase in the number of good quality of embryos obtained (p<0.05). After the treatment with DHEA, there was an improvement in the number of oocytes retrieved, Metaphase II (MII) oocyte (mature) oocytes obtained, fertilised and transferrable embryos and the pregnancy rate. There was no significant effect of DHEA treatment on the number of days of stimulation and cumulative dose of gonadotrophins used.
CONCLUSION: Our results is able to show that DHEA supplementation may help to enhance IVF-ICSI outcomes in women with POR especially in those age 35 years and below.

Matched MeSH terms: Oocytes/drug effects*
Anthelmintic resistance in goats in peninsular Malaysia

Dorny P, Claerebout E, Vercruysse J, Sani R, Jalila A

Vet Parasitol, 1994 Dec;55(4):327-42.
PMID: 7725626

Ninety-six randomly selected farms, located throughout peninsular Malaysia, were surveyed for goat nematodes resistant to benzimidazoles (BZ). On 33 farms BZ resistance was demonstrated by means of an egg hatch assay. Haemonchus contortus was found to be the main species involved in anthelmintic resistance. There was a positive association between the frequency of anthelmintic treatments on a farm and the presence of benzimidazole resistance. To assess the value of the egg hatch assay, faecal egg count reduction (FECR) tests were also performed on 20 farms. On six farms the LD50 of thiabendazole (TBZ) was less than 0.10 micrograms ml-1 and the FECR higher than 95% and on ten farms with an LD50 TBZ of over 0.10 micrograms ml-1 a FECR of less than 95% was measured. On four farms the FECR was less than 95%, although the egg hatch assay showed LD50 TBZ values of less than 0.10 micrograms ml-1 and on two of these three farms a controlled efficacy test confirmed the presence of BZ resistant H. contortus. From these results it can be concluded that the egg hatch assay underestimated the true incidence of benzimidazole resistance. Levamisole resistance was detected with a FECR test on two of ten farms investigated.

Matched MeSH terms: Oocytes/drug effects
Alanine to glycine substitution in the PyR2 confers sodium channel resistance to Type I pyrethroids

Chen M, Wang L, Zhou X, Chen G, Xu Z, Yan R, et al.

Pest Manag Sci, 2025 Apr;81(4):2248-2256.
PMID: 39740097 DOI: 10.1002/ps.8625

BACKGROUND: Aedes aegypti is a primary urban vector of dengue, yellow fever, Zika and chikungunya worldwide. Pyrethroid insecticides are the most effective insecticides for controlling Ae. aegypti. However, pyrethroid resistance has developed due to the long-term overuse of the insecticides, and many knockdown resistance (kdr) mutations have been identified in the resistant populations. A1007G, an alanine to glycine substitution, was found in resistant Ae. aegypti from Vietnam and Malaysia, which has always co-existed with F1534C and V1016G. However, the role of A1007G in pyrethroid resistance and the linkage of A1007G and F1534C or V1016G remain unknown.
RESULTS: In this study, we examined the effects of mutations on the sodium channel gating properties and pyrethroid sensitivity in Xenopus oocytes. We found mutations A1007G, A1007G + F1534C and A1007G + V1016G + F1534C shifted the voltage dependence of activation in the depolarizing direction. Mutations A1007G + F1534C and A1007G + V1016G + F1534C shifted the voltage dependence of inactivation in the depolarizing direction. Both mutations A1007G and F1534C reduced the channel sensitivity to two Type I pyrethroids, permethrin and bifenthrin, and synergistic effects were observed between mutations A1007G and F1534C. However, none of the mutations, A1007G, F1534C and A1007G + F1534C affected the channel sensitivity to two Type II pyrethroids, deltamethrin and cypermethrin. Furthermore, triple mutations A1007G + V1016G + F1534C significantly reduced the channel sensitivity to both Type I and Type II pyrethroids.
CONCLUSION: We identified A1007G had a distinct effect on sodium channel sensitivity to Type I, but not to Type II pyrethroids, also A1007G exhibited synergistic effects with F1534C to Type I pyrethroids, which will provide a fundamental insight into the distinct molecular interactions between insect sodium channel and Type I or Type II pyrethroids. © 2024 Society of Chemical Industry.

Matched MeSH terms: Oocytes/drug effects
Neuromuscular effects of candoxin, a novel toxin from the venom of the Malayan krait (Bungarus candidus)

Nirthanan S, Charpantier E, Gopalakrishnakone P, Gwee MC, Khoo HE, Cheah LS, et al.

Br J Pharmacol, 2003 Jun;139(4):832-44.
PMID: 12813007

1 Candoxin (MW 7334.6), a novel toxin isolated from the venom of the Malayan krait Bungarus candidus, belongs to the poorly characterized subfamily of nonconventional three-finger toxins present in Elapid venoms. The current study details the pharmacological effects of candoxin at the neuromuscular junction. 2 Candoxin produces a novel pattern of neuromuscular blockade in isolated nerve-muscle preparations and the tibialis anterior muscle of anaesthetized rats. In contrast to the virtually irreversible postsynaptic neuromuscular blockade produced by curaremimetic alpha-neurotoxins, the neuromuscular blockade produced by candoxin was rapidly and completely reversed by washing or by the addition of the anticholinesterase neostigmine. 3 Candoxin also produced significant train-of-four fade during the onset of and recovery from neuromuscular blockade, both, in vitro and in vivo. The fade phenomenon has been attributed to a blockade of putative presynaptic nicotinic acetylcholine receptors (nAChRs) that mediate a positive feedback mechanism and maintain adequate transmitter release during rapid repetitive stimulation. In this respect, candoxin closely resembles the neuromuscular blocking effects of d-tubocurarine, and differs markedly from curaremimetic alpha-neurotoxins that produce little or no fade. 4 Electrophysiological experiments confirmed that candoxin produced a readily reversible blockade (IC(50) approximately 10 nM) of oocyte-expressed muscle (alphabetagammadelta) nAChRs. Like alpha-conotoxin MI, well known for its preferential binding to the alpha/delta interface of the muscle (alphabetagammadelta) nAChR, candoxin also demonstrated a biphasic concentration-response inhibition curve with a high- (IC(50) approximately 2.2 nM) and a low- (IC(50) approximately 98 nM) affinity component, suggesting that it may exhibit differential affinities for the two binding sites on the muscle (alphabetagammadelta) receptor. In contrast, curaremimetic alpha-neurotoxins have been reported to antagonize both binding sites with equal affinity.

Matched MeSH terms: Oocytes/drug effects
Deleterious effects of nicotine on the ultrastructure of oocytes: role of gamma-tocotrienol

Rajikin MH, Latif ES, Mar MR, Mat Top AG, Mokhtar NM

Med Sci Monit, 2009 Dec;15(12):BR378-83.
PMID: 19946227

Previous studies have shown that nicotine enhances oxidative DNA damage and leads to increased lipid peroxidation, which affects embryo development. The present study investigated the effect of daily supplementation of gamma-tocotrienol on oocytes of nicotine-treated mice.

Matched MeSH terms: Oocytes/drug effects*