Abstract

     Despite the growing attention which green human resource management (GHRM) has been gaining, the field is still remarkably young, and conceptual clarity is yet to be attained. A bibliometric review of GHRM from 2010 to 2020 was conducted on the Web of Science and analyzed using the VOSviewer software package, version 1.6.16 developed by Van Eck and Waltman (Leiden, The Netherlands). The results show the exponential growth of this topic, although there seems to be no consensus regarding its definition, conceptualization and measurement. Concerning its conceptual development, GHRM seems to currently fit the second stage of development (evaluation and augmentation) of Reichers and Schneider’s three-stage model of the evolution of constructs. Future research seems to point in the direction of establishing the barriers separating GHRM from other human resource management topics, defining green practices and determining the antecedents and consequences of GHRM.

Introduction

     The economic growth of the last two centuries has represented prosperity and longevity for humanity. However, the impact of various industrial practices, reflected in pollution and the accumulation of waste and residues, is increasingly evident (IPCC 2018; Jackson et al. 2011). Climate change represents a new set of challenges, altering competitive and regulatory spheres, indirectly through global policy efforts to curb carbon emissions, and directly as a means of combating the unravelling consequences of extreme weather events (IPCC 2018). By invoking unprecedented changes in socio-economic systems, climate change makes it urgent for society to prepare and adapt in the face of new contingencies (Winn et al. 2011). With increasing regulatory and public pressure, more and more business entities are proactively implementing practices and strategic changes, such as investing in low-CO2 technologies and renewable energy, in order to transition to environmental sustainability (González-Benito and González-Benito 2006; IPCC 2018).

     The multidisciplinarity required to reduce organizational environmental footprints challenges the vision that this theme is restricted to environmental sciences, causing new fields of study to emerge in the areas of social research and management (Shrivastava and Berger 2010). In this sense, several related topics have been increasingly emphasized: corporate social responsibility (CSR), environmental management (EM), business ethics, socially responsible consumption and sustainability strategies, among others (Schuler et al. 2017; Shrivastava and Berger 2010).

Conclusions and Future Directions

     The bibliometric analysis of the literature produced between 2010 and 2020 highlights the importance of GHRM today as an expanding field, particularly from the second half of the decade. The purpose of GHRM is to actively participate in the creation of greener societal paths and respond to environmental and ecological issues from the organizational context. This HRM specialty refers to one of the most important challenges faced by humanity

     By mapping the existing literature streams—implementation of GHRM as a strand of EM, consequences at the organizational level and consequences at the employee level— tracing their contributions and development in the last decade, and identifying the construct development stage, this paper has met its objectives. In short, the results obtained suggest that the implementation of green practices in organizations will be reflected in lower levels of environmental pollution and contamination. Despite the emphasis on the repercussions of GHRM at work, it goes beyond the labor sphere, since green environmental values are transferable from context to context, i.e., green behaviors applied at work are reflected in personal life and vice versa. The fact that the evolution of the construct has been going beyond a concept focused only on EM demonstrates the consideration of employees endowed with unique strategic value and their decisive role in organizational sustainability. The resource-based view (Barney 1991) is a theoretical contribution that points in this direction (Yusliza et al. 2017).

Highlights

Abstract

Graphical abstract

Keywords

1. Introduction

2. Literature search strategy & statistics

3. Historical framework: early hormetic findings

4. Radiation – UV and ionizing

5. Pollution and pollen

6. Polyamines

7. Discussion

8. Conclusion

CRediT authorship contribution statement

Declaration of competing interest

Acknowledgement

Appendix A. Supplementary data

References

Abstract

This paper evaluated the occurrence of hormetic dose responses in pollen reported over the past eight decades. Hormetic doses responses were induced by a wide range of chemical and physical agents in 34 plant species for pollen germination and pollen tube growth/elongation. Agents inducing such hormetic dose/concentration responses in pollen included nutrients, growth-promoting agents, plant and animal hormones, toxic substances, including heavy metals such as cadmium, gaseous pollutants such as ozone, as well as ionizing and non-ionizing radiation. This paper provides further evidence for the broad generality of the hormesis dose response, supporting substantial prior findings that the hormetic response is independent of biological model, inducing agent, and endpoints measured. Given the widespread potential of inducing hormetic dose responses in pollen, these findings indicate the need to explore their emerging biological, ecological, agricultural, economic and public health implications.

1. INTRODUCTION

In flowering plants, the reproduction process is mediated by the pollen tube. This tubular structure provides the vehicle by which two immobile sperm cells are transported to the ovule, the location of two female reproduction cells (Sprunck, 2010; Dresselhaus and Franklin-Tong, 2013; Vogler et al., 2014). The pollen tube develops only after the pollen grain is transported, attaches, and then rehydrates on the receptive papillae that reside on the top of the stigma. After this process, the pollen grain becomes activated to form the so-called pollen tube, which may be characterized as a tubular protrusion that is chemically directed via complex physical and sensory processes through the pistil, eventually reaching the female gametophyte. At this point in the process, the male reproductive cells finally arrive at the target destination and initiate the process of fertilization (Palanivelu and Tsukamoto, 2012). Beyond their essential role in fertilization, pollen tubes are widely used to assess biological polarity, with broad applications to other cell types and biological processes. Of considerable theoretical and practical significance is that the pollen grain displays a self-organizing system that permits pollen to germinate, producing pollen tubes in vitro within an external signal mediated framework. The pollen germination rates, pollen tube growth rates, and final tube length are typically lower in in vitro studies than those observed in whole plants, most likely due to the absence of female factors that affect pollen germination, tube growth and growth directionality (Johnson and Presse, 2002; Chae and Lord, 2011). The selection of plants for pollen studies is affected by many species-specific processes as there are many factors that affect pollen tube growth, including the morphology of the reproductive tract (e.g. the stigma, style, the septum epidermis, and the funiculus). The nutrient containing extracellular matrix (ECM) contains a nutrient mixture that is important in enhancing pollen tube elongation Journal Pre-proof Journal Pre-proof 4 (Johnson and Presse, 2002; Chae and Lord, 2011). However, many studies employ bi-cellular pollen from species such as tobacco, which yields reliable findings (Volger et al., 2014).

1- Introduction

2- Methods

3- Results

4- Discussion

References

Abstract

Stress hormones have been shown to be important mediators in driving malignant growth and reducing treatment efficacy in breast cancer. Glucocorticoids can induce DNA damage through an inducible nitric oxide synthase (iNOS) mediated pathway to increase levels of nitric oxide (NO). Using an immune competent mouse breast cancer model and 66CL4 breast cancer cells we identified a novel role of NOS inhibition to reduce stress-induced breast cancer metastasis. On a mechanistic level we show that the glucocorticoid cortisol induces expression of keys genes associated with angiogenesis, as well as pro-tumourigenic immunomodulation. Transcriptomics analysis confirmed that in the lungs of tumour-bearing mice, stress significantly enriched pathways associated with tumourigenesis, some of which could be regulated with NOS inhibition. These results demonstrate the detrimental involvement of NOS in stress hormone signalling, and the potential future benefits of NOS inhibition in highly stressed patients.

Introduction

Psychological stress induces an increase in the circulating levels of stress hormones, including the glucocorticoid cortisol [1]. Epidemiological evidence has associated negative psychosocial factors, including chronic stress, with increased incidence and poorer survival in breast cancer patients [2]. Furthermore, multiple studies have linked psychological stress with biological processes involved in metastasis [3–5], findings of particular importance since the primary cause of breast cancer-related death is metastatic spread [6]. Glucocorticoid signalling, mediated through the glucocorticoid receptor (GR), has been shown to promote tumourigenesis and drug-resistance in triple negative breast cancer (TNBC) [7], and increases in expression of GR in breast tumours have been correlated with decreased survival [8]. GR antagonism has also previously been shown to induce apoptosis and, in combination with conventional chemotherapies, reduce tumour size in models of TNBC [9]. We have previously explored the mechanistic actions of psychological stress in breast cancer, and shown that stress hormone exposure can induce DNA damage in breast cancer through the generation of reactive oxygen and nitrogen species (ROS/RNS). We have also previously shown that glucocorticoids mediate a non-genomic effect on inducible nitric oxide synthase (iNOS), the enzyme that generates NO, and increase nitric oxide (NO) signalling in breast cancer cells [10]. Although iNOS is expressed in both ER+ and ER-breast cancers [11,12], expression of iNOS has been found to correlate with tumour progression and poor survival in basal-like breast cancers [13,14], indicating that NO activity may drive malignant growth and spread. As such, iNOS represents a potential target to abrogate the detrimental effects of psychological stress hormone signalling. Nitric oxide (NO) is an important signalling molecule modulating a range of functions within the cell, however the role of NO in tumour biology is complex and multifaceted [15]. Aspects of tumourigenic transformation can be driven by prolonged inflammation and exposure to high concentrations of NO, resulting in an increase in oxidative stress and subsequent DNA damage [16]. It is thought that NO may also be capable of driving transformation through the induction of angiogenesis and migration [17]. The highest concentrations of NO are produced by iNOS, and expression of iNOS has been shown to be positively correlated with tumour grade, stage and metastasis in breast cancer [11,18–20]. Several studies have shown that induction of iNOS expression in tumour cells promotes an increase in angiogenesis, and subsequently an increase in invasiveness and progression [16,21,22].

1- Introduction

2- Materials and methods

3- Results

4- Discussion

References

Abstract

Introduction
Prophylactic bilateral salpingo-oophorectomy (BSO) is recommended at an early age to BRCA mutation carriers to prevent ovarian cancer. It is critical to evaluate the impact of BSO on non-cancer outcomes, including quality of life (QOL), menopausal symptoms and sexual functioning.
Methods BRCA mutation carriers who elected to undergo a BSO completed three questionnaires prior to surgery and then again approximately one and three years following surgery which included: 1) medical history questionnaire, 2) Menopause-Specific Quality of Life Intervention questionnaire and 3) Sexual Activity Questionnaire. The change in quality of life, menopausal symptoms and sexual functioning before and after oophorectomy was determined using a paired t-test and stratified by menopausal status at surgery.
Results We included 140 BRCA mutation carriers with an average follow-up of 3.5 years following BSO. Among 93 women who were premenopausal, oophorectomy was associated with an increase in menopausal symptoms (vasomotor, physical) (P < 0.001) and a decline in sexual functioning (discomfort, pleasure) (P ≤ 0.0001), but had no impact on overall QOL (P = 0.31). HRT mitigated, but did not eliminate the adverse effects. Women who were postmenopausal at surgery (n = 47) experienced an increase in physical symptoms (P = 0.03) and a decline in sexual functioning (discomfort) (P = 0.004) and in overall QOL (P = 0.04).
Conclusions This study demonstrates that 3.5 years after oophorectomy, BRCA mutation carriers experience a significant worsening of menopausal symptoms and a decline in sexual functioning, particularly among those who underwent surgery prior to natural menopause. The use of HRT mitigated some but not all the effects. Overall, women who were premenopausal at surgery did not experience a decline in their QOL.

Introduction

Women with a BRCA1 or BRCA2 mutation face a high lifetime risk of developing ovarian cancer and preventive bilateral salpingooophorectomy (BSO) (referred to as oophorectomy hereafter) is recommended prior to menopause [1]. Screening for ovarian cancer in highrisk women has not been shown to be reliable and currently surgical risk reduction is the most effective option [2]. Oophorectomy is currently recommended between the ages of 35 and 40 for BRCA1 mutation carriers and between 40 and 45 for BRCA2 mutation carriers [1,3]. Oophorectomy reduces the risk of developing ovarian cancer as well as all-cause mortality [4]. Despite the well-established reduction in cancer risk, oophorectomy induces surgical menopause and its associated risks and sequelae. The abrupt decline in circulating sex hormones (e.g., estrogen, testosterone, and progesterone) causes menopausal symptoms, including vasomotor symptoms and loss of libido, and is associated with a decline in cardiac and bone health, and perhaps in memory and attention [5–7]. This may be most apparent among those women who undergo surgery prior to natural menopause. Many of the side effects can be ameliorated by hormonal replacement therapy (HRT), but for women with a personal history of breast cancer, exogenous hormones are contraindicated due to fear of recurrence [8]. To date, there have been few prospective studies among women with a BRCA mutation who represent a unique population given their high rate of surgical menopause [reviewed in [9,10]]. Women undergoing preventive surgery experience reduced cancerspecific distress and a sustained level of overall quality of life [10].

Although Attention-Deficit/Hyperactivity Disorder shows (ADHD) male predominance, females are significantly impaired and exhibit additional comorbid disorders during adolescence. However, no empirical work has examined the influence of cyclical fluctuating steroids on ADHD symptoms in women. The present study examined estradiol (E2), progesterone (P4), and testosterone (T) associations with ADHD symptoms across the menstrual cycle in regularlycycling young women (N=32), examining trait impulsivity as a moderator. Women completed a baseline measure of trait impulsivity, provided saliva samples each morning, and completed an ADHD symptom checklist every evening for 35 days. Results indicated decreased levels of E2 in the context of increased levels of either P4 or T was associated with higher ADHD symptoms on the following day, particularly for those with high trait impulsivity. Phase analyses suggested both an early follicular and early luteal, or post-ovulatory, increase in ADHD symptoms. Therefore, ADHD symptoms may change across the menstrual cycle in response to endogenous steroid changes.

Introduction

Attention-Deficit/Hyperactivity Disorder (ADHD) is a common and impairing childhood neurodevelopmental disorder (APA, 2013; Bernfort et al., 2008; Pelham et al., 2007, Polanczyk et al., 2007; Sayal et al. 2017; Thomas et al., 2015) that often persists into adolescence and adulthood with a prevalence of approximately 3% in adults (Faraone & Biederman, 2005; Fayyad et al., 2017; Kessler et al., 2006; Wilcutt, 2012). ADHD is a heterogeneous condition, currently conceptualized theoretically using multiple pathway models (Nigg et al., 2004; SonugaBarke, 2005) and most accurately described using two continuous symptom dimensions of inattention and hyperactivity-impulsivity (Haslam et al., 2006; Larsson et al., 2012; Marcus & Barry, 2011). Although ADHD is more frequently diagnosed in males, females with ADHD often become particularly impaired and exhibit comorbid disorders beginning during adolescence (Biederman et al., 1999; Hinshaw et al., 2012; Hosain, et al., 2012; Lahey et al. 1994; Quinn, 2005; Robison et al., 2008). The mechanisms of such sex differences remain unclear yet fundamental to understanding ADHD and sex differences in ADHD. Prior work suggests a role for organizational testosterone (T) in ADHD symptoms in both sexes (Wang et al., 2017), but particularly males (Martel, 2009; McFadden et al., 2005). Women and girls are under-studied and in particular, activational hormonal effects remain essentially unstudied in ADHD. Case studies have suggested that ADHD symptoms may worsen the week before menstruation (during declining estrogen and progesterone; Quinn, 2005) and improve during pregnancy (during elevated estrogen and progesterone (Nadeau & Quinn, 2002), but empirical work is lacking. Higher estradiol (E2) and progesterone (P4) have been generally linked to enhanced executive function (EF) and attention (e.g., Hatta & Nagaya, 2009), which appear to improve during cycle phases characterized by elevated E2 and P4 (Gogos, 2013; Howard et al., 1988; Jacobs & D’Esposito, 2011; Lord & Taylor, 1991; Rosenberg & Park, 2002; Segal, 2012; Vranic ́ & Hromatko, 2008; Solís-Ortiz & Corsi-Cabrera, 2008; Solis-Ortiz et al., 2004). Further, verbal fluency, verbal learning and memory appear to improve with administration of T in women (Davison et al., 2011; Drake et al., 2000), whereas response inhibition performance decreases (Bjork et al., 2001). Given that weak EF is a prominent correlate and possible marker of ADHD, this prior work suggests a potential role for cycling reproductive steroids in daily ADHD symptom expression.

The experimental study of the physiological mechanisms of animal behavior, which began in the 1800s, has dual origins. Research on neural mechanisms, now referred to as behavioral neurobiology, neuroethology, or behavioral neuroscience, has its roots in comparative neuroanatomy, comparative physiology, and physiological psychology. Research on hormonal mechanisms, now known as behavioral neuroendocrinology, arose from endocrinology in addition to many other fields. With the realization that the nervous and endocrine systems are functionally connected, there has been increased integration within the field. Connections with several newer branches of science, such as molecular biology, have been established as well.

Introduction

Two types of mechanisms, neural and hormonal, have been prominent in the history of research directed at uncovering the proximate physiological causes of animal behavior. During the first part of this history, the nervous and endocrine systems were envisioned as separate systems and were studied by somewhat different research communities. As a result, research on physiological mechanisms of animal behavior has tended to develop along two somewhat separate and parallel tracks. These dual origins are reflected in the organization of this survey. Beginning in the 20th century, several discoveries led to the realization that the nervous and endocrine systems are physiologically integrated to a highly significant extent, which is of great importance for animal behavior. Nerve cells can synthesize and secrete hormones; the behavioral effects of hormones are mediated by their actions on neurons, and the brain regulates the endocrine axes so that hormone levels related to behavior are responsive to both social and physical environments.

Origins of Behavioral Neurobiology: Sensory, Motor, and Motivational Systems in Comparative Perspective

The history of the study of the neural mechanisms of animal behavior is largely the history of neuroscience in a more general sense. The overarching motivation of the pioneers was often a desire to understand human minds and brains. However, because of the impossibility of doing experimental work with humans, investigations of animals have long played a significant role. The oldest and deepest scientific roots of the field are comparative neuroanatomy and comparative physiology. Then in the 20th century, developments in ethology led to the rise of neuroethology (also called behavioral neurobiology), which emphasized naturally occurring behavior in nondomesticated animals, while developments in psychology produced the subfield of physiological psychology, with its emphasis on learning, memory, and motivation in domesticated laboratory animals.

Melatonin, the ‘chemical signal of darkness’, is responsible to regulate biological rhythms and different physiological processes. It is mainly produced by the pineal gland as a hormone in a rhythmic daily basis, but it may also be synthesized by other tissues, such as immune cells, under inflammatory conditions. Its abnormal circulating levels have been related to several diseases such as type 2 diabetes, Alzheimer’s disease and some types of cancer. Currently, melatonin is exclusively quantified by ELISA or radioimmunoassays, which although are very sensitive techniques and present low detection limits, usually require specialized personal and equipment, restricting the tests to a limited number of patients. To overcome such limitations, we developed a novel easy-to-use electrochemical immunosensor for rapid melatonin quantification. Anti-melatonin antibodies were immobilized into Indium tin oxide (ITO) platforms using (3- Aminopropyl)triethoxysilane (APTES), 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide (EDC) and N-hydroxysuccinimide (NHS) crosslinkers. The platforms were assayed with synthetic and biologically-present melatonin containing samples. The developed device displayed a linear response in the concentration range from 0.75 to 7.5 µmol/L and a limit of detection of 0.175 µmol/L using Electrochemical Impedance Spectroscopy (EIS) (R2=0.989) and 0.513 µmol/L using Cyclic Voltammetry (CV) (R²=0.953) for synthetic melatonin. Furthermore, the sensors exhibited a good stability and reproducibility (3.45% and 2.87% for EIS and CV, respectively, n=3), maintaining adequate response even after 30 days of assembly. On biologically-present melatonin-containing samples the device displayed a similar performance when compared to ELISA technique (deviation of 13.31%). We expect that the developed device contributes significantly to the medical area allowing precise and complete diagnosis of the diseases related to abnormal levels of melatonin.

Introduction

Melatonin (N-acetyl-5-methoxy tryptamine) is an indoleamine present in most biological interfaces. In several species, melatonin plays important roles as a hormone and it is believed that its biological signaling is one of the oldest existing in nature.1 In humans, melatonin biosynthesis is rhythmically active in the pineal gland. Some other tissues, which includes the retina and gastrointestinal tract, may also synthesize melatonin in a rhythmic manner. 2 Melatonin may also be synthesized on demand by macrophages, lymphocytes and microglia when activated by pathogens or abiotic injuries.2-4 . Under normal conditions its maximum concentration in human plasma is about 50-200 pg/mL (0.22-0.86 nmol/L) during the night and lower than 2.0 pg/mL (8.6 pmol/L) at daylight, 5-7 which is in accordance with one of its major functions: translating environmental darkness to adjust endogenous physiology. Excretion of melatonin in the urine is also a pivotal marker of melatonin bioavailability. It is noteworthy to mention that melatonin can also be found in human saliva at concentrations ten times lower than in plasma, which highlights the possibility for the development of non-invasive and sensitive methods for detection of the indoleamine in different biological fluids. The idea that melatonin is only linked to the circadian rhythms or seasonal behavior was long challenged by the scientific community. In the last decades, intense efforts have been spent in understanding the influence of this hormone in other actions and physiological systems3,8-10 . For example, studies have shown that melatonin presents a very important role on the organization of the immune response11 . In this case, the hormone derived from the pineal gland is ceased but is locally produced by defense cells and acts locally, as regulator of the immune response. Also, under inflammatory frames, nocturnal pineal melatonin suppression favors the mounting of inflammation by allowing the rolling and adherence of leukocytes as well as its vascular permeability.

Introduction

Energy homeostasis is critical for life; therefore diverse hormonal mechanisms have evolved to regulate cellular energy utilization as well as inter-tissue communication to coordinate metabolic pathways. Although regulation of cellular metabolism by major controllers such as insulin and glucagon is well-established, a new distinct subgroup of fibroblast growth factors consisting of FGF19, FGF21 and FGF23, has been recently identified to play critical roles in the metabolic network. Within FGF superfamily, these three factors share the highest level of homology with one another and propagate their effects via FGFRs, although each of them displays a diverse mechanism of receptor activation. In contrast to classical FGFs that require heparin for efficient FGFR engagement, FGF19, FGF21 and FGF23 lack conventional heparin-binding domains. This property allows these factors to elude body’s vast depot of extracellular heparan sulphate proteoglycans and be readily present in the circulation, thus putatively function in an endocrine-like manner [1,2]. Despite the absence of heparin-binding domains, FGF19, FGF21 and FGF23 still require cofactors, type 1 transmembrane proteins Klotho [3] or βKlotho [4], for efficient FGFR activation [5–7]. In contrast to ubiquitously expressed FGFRs, patterns of Klotho and βKlotho expression in the body are fairly restricted. Thus, Klotho and βKlotho, not FGFRs, define tissue selectivity of action for the hormone-like FGFs and determine the distinct physiological roles of these factors: FGF19 regulates cholesterol/bile acid (BA) synthesis, FGF21 controls glucose and lipid metabolism, and FGF23 modulates phosphate/vitamin D metabolism [8–10].

Abstract

Purpose: Recurrent pregnancy loss (RPL) could be caused by insufficient progesterone in the luteal phase of menstruation and early pregnancy. Progesterone plays a critical role in oocyte maturation, embryo implantation and placenta maintenance in early gestation. This study was set out to investigate the association between polymorphisms of the progesterone receptor (PGR) gene and idiopathic RPL.

Methods: One hundred twenty-one women with a history of idiopathic recurrent pregnancy loss (RPL) and 179 control subjects were enrolled into the study. Six tag SNPs and two functional SNPs [PROGINS (rs1042838), +331 C/T (rs10895068)] of the progesterone receptor gene were genotyped.

Results: We found that the allele and genotype frequencies of the functional SNP [PROGINS (rs1042838)] were both significantly higher in patients with idiopathic RPL than in the control subjects (both P values = 0.006). In addition, the C-C haplotype, which consists of rs590688C > G and rs11224592T > C, is associated with a decreased risk of RPL (p = 0.004).

Conclusion: PROGINS polymorphism confers susceptibility to idiopathic recurrent pregnancy loss in Taiwanese Han women.

Introduction

The occurrence of repeated pregnancy loss (RPL) affects about 1–5% of couples [1]. RPL is a multifactorial disorder and various factors have been implicated, including uterine anomaly, chromosomal abnormalities, endocrine dysfunction, thrombophilia, immune disorders, lifestyle factors and maternal infections. However, the exact underlying causes remain undetermined in up to 50% of cases [2].

The thyroid hormones act on nearly every cell in the body. They act to increase the basal metabolic rate, affect protein synthesis and regulate long bone growth and neural maturation. The thyroid hormones are essential for the proper development and differentiation of all cells of the human body. The thyroid hormones also affect the female reproductive organs. In combination with follicle-stimulating hormone, triiodothyronine (T3) enhances granulosa cell proliferation and inhibits granulosa cell apoptosis by the phosphatidylinositol 3-kinase/Akt (also known as protein kinase B) pathway [1]. Leukemia inhibitory factor (LIF) is involved in the embryo implantation process and expressed in the mid-secretory endometrium [2]. Thyroid-stimulating hormone (TSH) significantly upregulates LIF expression in endometrial cell cultures, suggesting a potential role of TSH in the implantation process [3]. Moreover, T3 increases the expression of matrix metalloproteinases (MMP), MMP-2, MMP-3, fetal fibronectin, and integrin a5b1T3 in cultured early placental extravillous trophoblasts, suggesting that it plays a vital role in regulating the invasive potential of extravillous trophoblasts [4]. The thyroid hormones are involved in almost all phases of reproduction, from folliculogenesis to placentation. This review focuses on the interactions between thyroid dysfunctions and subfertility, as well as the proper work-up and management of thyroid dysfunctions in subfertile women.