Chromoionophoric molecular probe infused bimodal porous polymer rostrum as solid-state ocular sensor for the selective and expeditious optical sensing of ultra-trace toxic mercury ions.

This study presents a distinctive solid-state naked-eye colorimetric sensing approach by encapsulating a chromoionophoric probe onto a hybrid macro-/meso-pore polymer scaffold for fast and selective sensing of ultra-trace Hg(II). The customized structural/surface properties of the poly(VPy-co-TM) monolith are attained by specific proportions of 2-vinylpyridine (VPy), trimethylolpropane trimethacrylate (TM), and pore-tuning solvents. The interconnected porous network of poly(VPy-co-TM), inherent superior surface area and porosity, is captivating for the homogeneous/voluminous incorporation of probe molecules, i.e., 7-((4-methoxyphenyl)diazenyl)quinoline-8-ol (MPDQ), for the target-specific colorimetric detection. The structural morphology, surface topography, and phase characteristics of the bare poly(VPy-co-TM) monolith and MPDQ@poly(VPy-co-TM) sensor are examined using HR-TEM-SAED (High-Resolution Transmission Electron Microscopy - Selected Area Electron Diffraction), FE-SEM-EDAX (Field Emission Scanning Electron Microscopy - Energy Dispersive X-ray Spectroscopy), XPS (X-ray Photoelectron Spectroscopy), p-XRD (Powder X-Ray Diffraction), FT-IR (Fourier Transform Infrared Spectroscopy), UV-Vis-DRS (Ultraviolet-Visible Diffuse Reflectance Spectroscopy), and BET/BJH (Brunauer-Emmett-Teller / Barrett-Joyner-Halenda) analysis. The distinctive properties of the sensor reveal a constrained geometrical orientation of the MPDQ probe onto the long-range continuous monolithic network of meso-/-macropore template, enabling selective interaction with Hg(II) with peculiar color transfiguration from pale yellow to deep brown. The sensor demonstrates a linear spectral-color alliance in the 0-200 ppb concentration range for Hg(II), with quantification and detection limits of 0.63 and 0.19 ppb. The sensor efficacy is verified using certified contaminated water and tobacco samples, with excellent reusability, reliability, and reproducibility of ≥ 99.23 % (RSD ≤1.89 %) and ≥ 99.19 % (RSD ≤1.94 %) of Hg(II), respectively.

Targeting the paracrine hormone-dependent guanylate cyclase/cGMP/phosphodiesterases signaling pathway for colorectal cancer prevention.

Colorectal cancer (CRC) is one of the leading causes of cancer related-deaths. The risk of development of CRC is complex and multifactorial, and includes disruption of homeostasis of the intestinal epithelial layer mediated though dysregulations of tumor suppressing/promoting signaling pathways. Guanylate cyclase 2C (GUCY2C), a membrane-bound guanylate cyclase receptor, is present in the apical membranes of intestinal epithelial cells and maintains homeostasis. GUCY2C is activated upon binding of paracrine hormones (guanylin and uroguanylin) that lead to formation of cyclic GMP from GTP and activation of downstream signaling pathways that are associated with normal homeostasis. Dysregulation/suppression of the GUCY2C-mediated signaling promotes CRC tumorigenesis. High-calorie diet-induced obesity is associated with deficiency of guanylin expression and silencing of GUCY2C-signaling in colon epithelial cells, leading to tumorigenesis. Thus, GUCY2C agonists, such as linaclotide, exhibit considerable role in preventing CRC tumorigenesis. However, phosphodiesterases (PDEs) are elevated in intestinal epithelial cells during CRC tumorigenesis and block GUCY2C-mediated signaling by degrading cyclic GMP to 5`-GMP. PDE5-specific inhibitors, such as sildenafil, show considerable anti-tumorigenic potential against CRC by amplifying the GUCY2C/cGMP signaling pathway, but cannot achieve complete anti-tumorigenic effects. Hence, dual targeting the elevation of cGMP by providing paracrine hormone stimuli to GUCY2C and by inhibition of PDEs may be a better strategy for CRC prevention than alone. This review delineates the involvement of the GUCY2C/cGMP/PDEs signaling pathway in the homeostasis of intestinal epithelial cells. Further, the events are associated with dysregulation of this pathway during CRC tumorigenesis are also discussed. In addition, current updates on targeting the GUCY2C/cGMP/PDEs pathway with GUCY2C agonists and PDEs inhibitors for CRC prevention and treatment are described in detail.

Development of the Smartphone-Assisted Colorimetric Detection of Thorium by Using New Schiff's Base and Its Applications to Real Time Samples.

In this paper, a new Th4+ ion-selective chromogenic sensor (L) was developed by reacting 1,10-phenanthroline-2,9-dicarbohydrazide with 2-hydroxy naphthaldehyde. The sensing ability of L toward Th4+ was investigated in solution and paper strips loaded with L using spectrophotometric and colorimetric methods. The selective interaction of L was examined with various f-metal ions and other selected metal ions from s-block and d-block elements. Results show that by the colorimetric method in solution-phase dimethyl sulfoxide/H2O (7:3, v/v) and paper strip methods, the naked-eye detectable color change of L occurred from colorless solution to yellow-orange and pale yellow colour upon interacting with Th4+ and Al3+, respectively, whereas other metal ions did not interfere. The ligand L exhibits two absorbance bands at 320 and 375 nm because of ligand-to-ligand charge transfer. Upon interaction with Th4+, L undergoes red shift of both absorption bands and the formation of a new UV-vis band at 335 and 440 nm. The UV-visible spectral studies indicate the formation of a 1:1 host-guest complex between L and Th4+ with an association constant of 4.7 × 103 M-1. The limit of quantification and limit of detection of L for the analysis of Th4+ are found to be 167 and 50 nM, respectively. The visually detectable color change of L has been well integrated with a smartphone RGB color value to make it an analytical signal for real-time analysis of Th4+ with the detection limit down to 116 nM. Besides, L was applied for the analysis of Th4+ content present in various real water samples, monazite, and lantern mantle samples by spectrophotometry and RGB color values. The binding mode of L with Th4+ is investigated by 1H NMR, electrospray ionization-mass, and theoretical studies.

Protective Effects of Human Chorionic Gonadotropin Against Breast Cancer: How Can We Use This Information to Prevent/Treat the Disease?

Breast cancers (BCs) are the most common malignancies among women worldwide. Giving birth to a first child before 24 years of age decreases the BC risk by about half, when women reach menopausal years. The scientific evidence suggests that the actions of human chorionic gonadotropin (hCG) are responsible for this decrease. Human BC cells and tissues contain hCG/luteinizing hormone receptors. The activation of the receptors results in an increase in cell differentiation and apoptosis. Conversely, it decreases the cell proliferation, invasion, and survival. The hCG actions are primarily cyclic adenosine monophosphate/protein kinase A mediated, require the presence of receptors, and involve blocking the activation and nuclear translocation of the transcription factor, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). The women with a higher hCG levels during pregnancy tend to have a lower BC incidence and those with the receptor-positive tumors have a longer metastasis-free survival. The long-term benefits of pregnancy/hCG seem to come from permanent signature genomic imprinting and expression changes, which are characterized by low cell proliferation, increased efficiency of DNA repair mechanisms, cell differentiation, and cells resistance to carcinogenesis. These findings could provide clinical opportunities to use hCG for the prevention of BC in this modern era of increasing number of young women in our societies waiting longer than ever to have their first child. In addition, hCG may be useful to reduce and/or eliminate cellular targets of carcinogenic changes during an active ongoing disease.

Involvement of Luteinizing Hormone in Alzheimer Disease Development in Elderly Women.

Alzheimer disease (AD) is a slow progressive neurodegenerative disease that affects more elderly women than elderly men. It impairs memory, typically progresses into multidomain cognitive decline that destroys the quality of life, and ultimately leads to death. About 5.3 million older Americans are now living with this disease, and this number is projected to rise to 14 million by 2050. Annual health-care costs in the United States alone are projected to increase to about US$1.1 trillion by 2050. The initial theory that decreasing estrogen levels leads to AD development in postmenopausal women has been proven inconclusive. For example, Women's Health Research Initiative Memory Study and the population-based nested case-control study have failed to demonstrate that estrogen/progesterone (hormone replacement therapy [HRT]) or estrogen replacement therapy could prevent the cognitive decline or reduce the risk of AD. This led to the realization that AD development could be due to a progressive increase in luteinizing hormone (LH) levels in postmenopausal women. Accordingly, a large number of studies have demonstrated that an increase in LH levels is positively correlated with neuropathological, behavioral, and cognitive changes in AD. In addition, LH has been shown to promote amyloidogenic pathway of precursor protein metabolism and deposition of amyloid ß plaques in the hippocampus, a region involved in AD. Cognate receptors that mediate LH effects are abundantly expressed in the hippocampus. Reducing the LH levels by treatment with gonadotropin-releasing hormone agonists could provide therapeutic benefits. Despite these advances, many questions remain and require further research.

The Luteinizing Hormone-Testosterone Pathway Regulates Mouse Spermatogonial Stem Cell Self-Renewal by Suppressing WNT5A Expression in Sertoli Cells.

Spermatogenesis originates from self-renewal of spermatogonial stem cells (SSCs). Previous studies have reported conflicting roles of gonadotropic pituitary hormones in SSC self-renewal. Here, we explored the role of hormonal regulation of SSCs using Fshb and Lhcgr knockout (KO) mice. Although follicle-stimulating hormone (FSH) is thought to promote self-renewal by glial cell line-derived neurotrophic factor (GDNF), no abnormalities were found in SSCs and their microenvironment. In contrast, SSCs were enriched in Lhcgr-deficient mice. Moreover, wild-type SSCs transplanted into Lhcgr-deficient mice showed enhanced self-renewal. Microarray analysis revealed that Lhcgr-deficient testes have enhanced WNT5A expression in Sertoli cells, which showed an immature phenotype. Since WNT5A was upregulated by anti-androgen treatment, testosterone produced by luteinizing hormone (LH) is required for Sertoli cell maturation. WNT5A promoted SSC activity both in vitro and in vivo. Therefore, FSH is not responsible for GDNF regulation, while LH negatively regulates SSC self-renewal by suppressing WNT5A via testosterone.

Systemic chromosome instability in Shugoshin-1 mice resulted in compromised glutathione pathway, activation of Wnt signaling and defects in immune system in the lung.

Mitotic error-mediated chromosome instability (CIN) can lead to aneuploidy, chromothripsis, DNA damage and/or whole chromosome gain/loss. CIN may prompt rapid accumulation of mutations and genomic alterations. Thus, CIN can promote carcinogenesis. This CIN process results from a mutation in certain genes or environmental challenge such as smoking, and is highly prevalent in various cancers, including lung cancer. A better understanding of the effects of CIN on carcinogenesis will lead to novel methods for cancer prevention and treatment. Previously Shugoshin-1 (Sgo1(-/+)) mice, a transgenic mouse model of CIN, showed mild proneness to spontaneous lung and liver cancers. In this study, adoptive (T/B-cell based) immunity-deficient RAG1(-/-) Sgo1(-/+) double mutant mice developed lung adenocarcinomas more aggressively than did Sgo1(-/+) or RAG1(-/-) mice, suggesting immune system involvement in CIN-mediated lung carcinogenesis. To identify molecular causes of the lung adenocarcinoma, we used systems biology approach, comparative RNAseq, to RAG1(-/-) and RAG1(-/-) Sgo1(-/+). The comparative RNAseq data and follow-up analyses in the lungs of naive Sgo1(-/+) mice demonstrate that, (i) glutathione is depleted, making the tissue vulnerable to oxidative stress, (ii) spontaneous DNA damage is increased, (iii) oncogenic Wnt signaling is activated, (iv) both major branches of the immune system are weakened through misregulations in signal mediators such as CD80 and calreticulin and (v) the actin cytoskeleton is misregulated. Overall, the results show multi-faceted roles of CIN in lung carcinoma development in Sgo1(-/+) mice. Our model presents various effects of CIN and will help to identify potential targets to prevent CIN-driven carcinogenesis in the lung.

Characterization of polycyclic aromatic hydrocarbons in fugitive PM10 emissions from an integrated iron and steel plant.

Fugitive emissions of PM10 (particles <10µm in diameter) and associated polycyclic aromatic hydrocarbons (PAHs) were monitored in the vicinity of coking unit, sintering unit, blast furnace and steel manufacturing unit in an integrated iron and steel plant situated in India. Concentrations of PM10, PM10-bound total PAHs, benzo (a) pyrene, carcinogenic PAHs and combustion PAHs were found to be highest around the sintering unit. Concentrations of 3-ring and 4-ring PAHs were recorded to be highest in the coking unit whereas 5-and 6-ring PAHs were found to be highest in other units. The following indicatory PAHs were identified: indeno (1,2,3-cd) pyrene, dibenzo (a,h) anthracene, benzo (k) fluoranthene in blast furnace unit; indeno (1,2,3-cd) pyrene, dibenzo (a,h) anthracene, chrysene in sintering unit; Anthracene, fluoranthene, chrysene in coking unit and acenaphthene, fluoranthene, fluorene in steel making unit. Total-BaP-TEQ (Total BaP toxic equivalent quotient) and BaP-MEQ (Total BaP mutagenic equivalent quotient) concentration levels ranged from 2.4 to 231.7ng/m(3) and 1.9 to 175.8ng/m(3), respectively. BaP and DbA (dibenzo (a,h) anthracene) contribution to total-BaP-TEQ was found to be the highest.

Therapeutic Potential of Human Chorionic Gonadotropin Against Painful Bladder Syndrome/Interstitial Cystitis.

Painful bladder syndrome/interstitial cystitis is a debilitating chronic bladder disease that primarily affects women. The disease is due to a damage of urothelial cell lining. As a result, potassium particles and other toxic substances in urine can leak into bladder mucosa, causing the symptoms of lower abdominal/pelvic discomfort, pain, increased urination frequency, urgency, nocturia, and so on, all of which can substantially reduce the quality of daily life. There are multiple symptom reliving therapies. Among them, only pentosan polysulfate sodium, sold under the brand name of Elmiron, has been approved for oral use by US Food and Drug Administration. It provides the relief after several months of use. Based on the scientific leads presented in this article, we propose that human chorionic gonadotropin has a therapeutic potential that is worth investigating for the treatment of this disease.

The Presence of Human Chorionic Gonadotropin/Luteinizing Hormone Receptors in Pancreatic ß-Cells.

We investigated the possible presence of functional human chorionic gonadotropin (hCG)/luteinizing hormone (LH) receptors in ß-cells of pancreas, using a combination of techniques on hCG/LH receptor knockout mice, immortalized rat insulinoma cells, and human pancreatic islets. The results showed the presence of receptors and their activation resulted in a dose-dependent increase in glucose-induced release of insulin. These findings place hCG and LH among the regulators of insulin release with potential implications for insulin-level changes during the periods of altered hCG and LH secretion.

Assessment of organochlorine pesticide residues in Indian flue-cured tobacco with gas chromatography-single quadrupole mass spectrometer.

Presence of pesticide residues in tobacco increases health risk of both active and passive smokers, apart from the imminent potential health problems associated with it. Thus, monitoring of pesticide residue is an important issue in terms of formulating stringent policies, enabling global trade and safeguarding the consumer's safety. In this study, a gas chromatography-single quadrupole mass spectrometry (GC-MS) method based upon quantifier-qualifier ions (m/z) ratio was employed for detecting and assessing ten organochlorine pesticide residues (α-HCH, ß-HCH, γ-HCH, δ-HCH, 2,4-DDT, 4,4-DDT, endrin, α-endosulfan, ß-endosulfan and endosulfan sulphate) in 152 flue-cured (FC) tobacco leave samples from two major tobacco growing states, Karnataka and Andhra Pradesh, of India. In the majority of samples, pesticide residue levels were below the limit of quantification (LOQ). In few samples, pesticide residues were detected and they found to comply with the guidance residue levels (GRL) specifications of the Cooperation Center for Scientific Research Relative to Tobacco (CORESTA). Detection of the phase out pesticides like DDT/HCH might be due to transfer of persistent residues from the environmental components to the plant. This is the first report on these ten organochlorine pesticide residues in Indian FC tobacco.

Antibiotic targeting of the bacterial secretory pathway.

Finding new, effective antibiotics is a challenging research area driven by novel approaches required to tackle unconventional targets. In this review we focus on the bacterial protein secretion pathway as a target for eliminating or disarming pathogens. We discuss the latest developments in targeting the Sec-pathway for novel antibiotics focusing on two key components: SecA, the ATP-driven motor protein responsible for driving preproteins across the cytoplasmic membrane and the Type I signal peptidase that is responsible for the removal of the signal peptide allowing the release of the mature protein from the membrane. We take a bird's-eye view of other potential targets in the Sec-pathway as well as other Sec-dependent or Sec-independent protein secretion pathways as targets for the development of novel antibiotics. This article is part of a Special Issue entitled: Protein trafficking and secretion in bacteria. Guest Editors: Anastassios Economou and Ross Dalbey.

Transcriptome analysis reveals new insights into the modulation of endometrial stromal cell receptive phenotype by embryo-derived signals interleukin-1 and human chorionic gonadotropin: possible involvement in early embryo implantation.

The presence of the conceptus in uterine cavity necessitates an elaborate network of interactions between the implanting embryo and a receptive endometrial tissue. We believe that embryo-derived signals play an important role in the remodeling and the extension of endometrial receptivity period. Our previous studies provided original evidence that human Chorionic Gonadotropin (hCG) modulates and potentiates endometrial epithelial as well as stromal cell responsiveness to interleukin 1 (IL1), one of the earliest embryonic signals, which may represent a novel pathway by which the embryo favors its own implantation and growth within the maternal endometrial host. The present study was designed to gain a broader understanding of hCG impact on the modulation of endometrial cell receptivity, and in particular, cell responsiveness to IL1 and the acquisition of growth-promoting phenotype capable of receiving, sustaining, and promoting early and crucial steps of embryonic development. Our results showed significant changes in the expression of genes involved in cell proliferation, immune modulation, tissue remodeling, apoptotic and angiogenic processes. This points to a relevant impact of these embryonic signals on the receptivity of the maternal endometrium, its adaptation to the implanting embryo and the creation of an environment that is favorable for the implantation and the growth of this latter within a new and likely hostile host tissue. Interestingly our data further identified a complex interaction between IL1 and hCG, which, despite a synergistic action on several significant endometrial target genes, may encompass a tight control of endogenous IL1 and extends to other IL1 family members.

Human chorionic gonadotropin regulates endothelial cell responsiveness to interleukin 1 and amplifies the cytokine-mediated effect on cell proliferation, migration and the release of angiogenic factors.

PROBLEM: Successful embryonic implantation requires an appropriate communication network between the embryo and its near environment within the implantation site. Herein, we examined whether human chorionic gonadotropin (hCG), the major embryonic signal, targets endothelial cells and regulate their responsiveness to interleukin 1 (IL1), one of the earliest signals released by embryonic cells. METHOD OF STUDY: Human microvascular endothelial cell proliferation and migration following exposure to various concentrations of hCG and/or IL1B for different time periods were analyzed by BrdU incorporation and wound healing assays. The expression of soluble (s) and membrane-bound (mb) IL1 receptors (IL1Rs), IL1R antagonist (IL1RN), luteinizing hormone/choriogonadotropin receptor (LHCGR), and IL8 was determined by real-time PCR, Western blot, and ELISA. RESULTS: Cell proliferation and migration increased in response to IL1B and further in the presence of hCG. IL1B up-regulated both the signaling IL1R1 and the inhibitory IL1R2, while adding hCG further increased IL1R1 and significantly downregulated IL1R2. This translated into an increased secretion of IL8, which was inhibited in cells where IL1R2 was overexpressed. CONCLUSIONS: These findings reveal a new mechanism by which hCG may target endothelial cells to directly stimulate angiogenesis and favor embryonic growth.

Human chorionic gonadotropin triggers angiogenesis via the modulation of endometrial stromal cell responsiveness to interleukin 1: a new possible mechanism underlying embryo implantation.

Deep functional changes occurring within the endometrium during implantation are orchestrated by embryonic and maternal signals. Human chorionic gonadotropin (hCG), a major embryonic signal, plays a critical role in the initiation and maintenance of pregnancy. Interleukin (IL) 1, one of the earliest embryonic signals, appears to exert a direct impact on the receptive endometrium and to induce major molecular changes that are essential for embryo implantation. Herein we investigate whether hCG can modulate endometrial stromal cell (ESC) receptivity to IL1 during the implantation window and assess the impact on angiogenesis in vitro. Primary cultures of ESCs from normal fertile women during the implantation window were treated for 24 h with different concentrations of hCG (0-100 ng/ml) and stimulated for 24 h with IL1B (0-0.1 ng/ml). IL1 receptors (IL1Rs), IL1R antagonist (IL1RA), and monocyte chemotactic protein (MCP) 1 were analyzed by real-time PCR, ELISA, and Western blotting. The angiogenic activity in vitro was studied using human microvascular endothelial cell line, scratch wound assay, and cell proliferation via BrdU incorporation into DNA. Human CG induced a dose-dependent imbalance in ESC receptivity to IL1 by significantly upregulating the functional signaling IL1R1 and concomitantly downregulating the decoy inhibitory IL1R2 and IL1RA upon subsequent exposure to IL1B. Prior exposure to hCG amplified MCP1 secretion by ESCs in response to IL1B and triggered the release of angiogenic activity in vitro in which MCP1 appeared to play a significant role. Overexpression of IL1R2 using cell transfection inhibited IL1 and hCG/IL1B-mediated MCP1 secretion. These findings suggest that hCG coordinates embryonic signal interaction with the maternal endometrium, and point to a new possible pathway by which it may promote embryonic growth.

Prophylactic vaccine approach for colon and pancreatic cancers: present and future.

Vaccines against cancers have not been as effective as vaccines against infectious diseases. However, recent studies have advanced our understanding of the stages of tumor cell development and of mechanisms of immune surveillance, immune suppression, and of tumor escape from the immune system. The development of animal models that mimic development of human cancers has helped advance the understanding of these processes and is aiding the development of greatly improved vaccines. Here we review the recent progress in developing vaccines and prophylactic approaches for pancreatic and colon cancers. Improved understanding of the expression of various oncogenes and tumor-associated antigens helps in selecting antigenic targets for stage-specific immune prevention. Identification of the earliest alterations in precancerous lesions and selection of epitopes unique to the aberrant cells and capable of triggering strong cytotoxic and helper T cell responses may aid the development of safe and effective vaccines for use in those at high risk of progressing to invasive cancers. The responses can be enhanced with carefully selected adjuvants to boost immunity and by selecting epitopes that are expressed on dendritic cells, thereby promoting T cell responses. Tumor resistance via loss of the targeted antigen can be mitigated by inclusion of multiple tumor epitopes in vaccine constructs. Tumor immune escape can be diminished by targeting various immunosuppressive mechanisms used by different tumors, such as tumor production of immunosuppressive cytokines (e.g., interleukin 10, and Transforming Growth Factor-beta, which can promote activity of immunosuppressive regulatory T cells), or by inhibiting production of inflammatory prostanoids with combined cyclooxygenase/lipoxygenase inhibitors. Finally, prevention of many cancers may be enhanced by carefully selecting and scheduling of vaccine administration in combination with other chemotherapeutic or chemopreventive agents. Preclinical and early clinical trials incorporating these principles are discussed.

Early detection and prevention of pancreatic cancer: use of genetically engineered mouse models and advanced imaging technologies.

Lack of early detection and effective interventions are major factors contributing to the poor prognosis and dismal survival rates of pancreatic cancer patients for more than sixty years. Detection of pancreatic cancer at an early stage might permit life-saving intervention. Clinical and preclinical diagnosis and evaluation of pancreatic cancers involve several imaging technologies including magnetic resonance imaging (MRI), Positron emission tomography (PET), Computed tomography (CT), Ultrasound (US), bioluminescent imaging and single photon emission computed tomography (SPECT). The advent of genetically engineered animal models that recapitulate the cellular and molecular pathology of human pancreatic intraepithelial neoplasia (PanINs) and pancreatic ductal adenocarcinoma (PDAC) has not yet yielded translational implications. Although the use of tumor xenografts to predict drug efficacy in patients has been disappointing, use of novel transgenic mice models should permit improved early detection and development of drug regimens through integration of appropriate imaging modalities. This review will consider issues that are unique to working with transgenic mouse models, such as the biology of genetically engineered mouse (GEM) models, stage- tumor-specific detection using imaging technologies, use of monoclonal antibodies, nanoparticles, and biomarkers, and development of chemopreventive and chemotherapeutic drugs for PDAC. These issues will be considered in the context of recently developed preclinical models of pancreatic cancer.

Can traumatic occlusion cause endodontic problems? A case report.

Radicular cysts are commonly found odontogenic cysts in the jaws. The lesion is diagnosed mainly in young patients during the second decade of life. In the majority of cases, it is asymptomatic. This paper reports a rare case in which traumatic occlusion was identified as the etiology of a radicular cyst. Endodontic treatment was performed and the traumatic occlusion also was corrected. A six-month follow-up appointment found good healing of the periapical region.

Virilization of a female infant by a maternal adrenocortical carcinoma.

OBJECTIVE: To describe a possible mechanism underlying the partial virilization of a 46, XX infant by a functional maternal adrenocortical carcinoma (ACC). METHODS: We performed immunocytochemical staining of tumor sections for luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptors. In addition, related reports in the literature are discussed. RESULTS: A previously healthy mother developed a large cortisol- and androgen-producing stage III adrenal tumor that did not interfere with conception or early morphogenesis. The tumor eluded detection until after delivery of a partially virilized 46, XX female infant with ambiguous genitalia. Immunohistochemical staining of tumor sections revealed overexpression of the LH/hCG receptor. Virilization of the genetically female fetus may have resulted from hCG-stimulated steroid secretion by the ACC. CONCLUSION: Because hypercortisolism and hyperandrogenism are associated with menstrual disturbances and spontaneous abortion, pregnancy in patients with functional adrenal tumors is uncommon. Rarely, maternal steroid excess from a functional adrenal tumor has caused 46, XX disordered sex differentiation. This unusual case demonstrates the influence of hCG on the functionality of an ACC and demonstrates the rare phenomenon of virilization of a female infant by a functional maternal adrenal tumor.