Atrazine is a potent endocrine disruptor that both chemically castrates and feminizes male amphibians. It depletes androgens in adult frogs and reduces androgen-dependent growth of the larynx in developing male larvae. It also disrupts normal gonadal development and feminizes the gonads of developing males. Gonadal malformations induced by atrazine include hermaphrodites and males with multiple testes [single sex polygonadism (SSP)], and effects occur at concentrations as low as 0.1 ppb (μg/L). Here, we describe the frequencies at which these malformations occur and compare them with morphologies induced by the estrogen, 17β-estradiol (E2), and the antiandrogen cyproterone acetate, as a first step in testing the hypothesis that the effects of atrazine are a combination of demasculinization and feminization. The various forms of hermaphroditism did not occur in controls. Nonpigmented ovaries, which occurred at relatively high frequencies in atrazine-treated larvae, were found in four individuals out of more than 400 controls examined (1%). Further, we show that several types of gonadal malformations (SSP and three forms of hermaphroditism) are produced by E2 exposure during gonadal differentiation, whereas a final morphology (nonpigmented ovaries) appears to be the result of chemical castration (disruption of androgen synthesis and/or activity) by atrazine. These experimental findings suggest that atrazine-induced gonadal malformations result from the depletion of androgens and production of estrogens, perhaps subsequent to the induction of aromatase by atrazine, a mechanism established in fish, amphibians, reptiles, and mammals (rodents and humans).
We describe a case of a progressive subcutaneous Alternaria alternata infection in the hand of a patient with chronic lymphocytic leukemia (CLL). The diagnosis was based upon the examination of tissue biopsy and isolation of the etiologic agent in culture. The identity of the isolate was determined by phenotypic characteristics and by sequencing the ITS and D1/D2 regions of the rDNA. Despite combination therapy with voriconazole and micafungin, the lesion continued to progress. Posaconazole therapy, along with surgical excision of the infected tissue, resulted in the eradication of infection. The limitations of the clinical management of invasive Alternaria infections are discussed.
Blepharoplasty, the most common aesthetic eyelid procedure, sometimes involves a challenging patient subgroup: those who present with malar edema, malar bags, and festoons. In this review article, the authors describe the relevant anatomy in festoon development, discuss the pathophysiological basis of this condition spectrum, outline clinical examination basics, summarize various surgical approaches for treatment and propose an algorithm for their application, and describe the most common postsurgical complications.
We report a 19-year-old, non-Amish Caucasian female patient with primary amenorrhea caused by complete lack of Müllerian fusion with vaginal agenesis or Müllerian aplasia (MA), postaxial polydactyly (PAP), and tetralogy of Fallot. The genital tract anomaly of MA with and without renal or skeletal anomalies comprises Mayer-Rokitansky-Kuster-Hauser syndrome, which has not been reported with tetralogy of Fallot. The phenotypic triad of anomalies most closely resembled McKusick-Kaufman syndrome (MKS; OMIM 236700), a rare multiple congenital anomaly syndrome comprised of hydrometrocolpos (HMC), PAP, and congenital heart malformation that is inherited in an autosomal recessive pattern. While upper reproductive tract anomalies have not been reported with MKS, they have been reported with Bardet-Biedl syndrome (BBS), a syndrome that significantly overlaps with MKS. Both MKS and BBS can be caused by mutations in the MKKS or BBS6 gene on chromosome 20p12 and BBS is also associated with mutations in other genes (BBS1, BBS2, BBS4, and BBS7). To address this heterogenity, we sequenced the causative genes in MKS and BBS but no mutations in these five genes were identified. Fluorescence in situ hybridization (FISH) excluded large deletions of chromosome 20p12 and microsatellite marker studies confirmed biparental inheritance for all of the known BBS loci. The dual midline fusion defects of tetralogy of Fallot and MA suggests that either this patient has a unique syndrome with a distinct genetic etiology or that she has a genetically heterogeneous or variant form of MKS.
Miniabdominoplasty with umbilical free float has received little attention in the literature in 15 years and has been criticized for an abnormally low umbilicus. We hypothesized the umbilicus in women presenting for abdominal contouring is positioned higher than ideal and thus may benefit from lowering. In addition, we felt modifications of the original umbilical float technique would improve aesthetic results. A retrospective review identified 60 patients aged 34 to 56 who had abdominoplasty with umbilical fascial transection and inferior positioning. Technical modifications included low placement of a full transverse abdominal scar, abdominal flap undermining to the rib cage, more inferior umbilical repositioning, flank liposuction, and plication of diastasis recti from xiphoid to pubis. Patients did not have enough excess skin to allow traditional abdominoplasty without a high-transverse or vertical midline scar. No umbilical or incisional skin necrosis occurred. To assess optimal umbilical position, plastic surgeons were asked to draw the ideal position on pre- and postoperative photographs from 5 patients. The mean ideal umbilical position was 2.2 cm lower than the actual position (P< 0.01) in preoperative photographs and was close to the true position in postoperative photographs. In conclusion, lower abdominoplasty with inferior umbilical positioning is an excellent choice for the middle age, postpartum woman with excess abdominal skin and full length diastasis recti but a normal body mass index.
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