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Resumen Introduccion El «sindrome del empujador» es un sindrome poco conocido que aparece tras sufrir un accidente cerebrovascular (entre el 10 y el 35% de los casos). Su presencia dificulta la recuperacion ya que el paciente considera su cuerpo vertical cuando esta inclinado unos 20° hacia el lado plejico. Antecedentes y objetivo Se trata de exponer el caso de una mujer, residente en un centro de personas mayores, que presenta dicho sindrome tras un accidente isquemico de la arteria cerebral media derecha. Descripcion del caso Mujer de 81 anos, diestra, autonoma para la marcha previamente a la lesion. Tras la lesion, se enfrenta a una situacion de dependencia, con graves alteraciones posturales. Intervencion Despues conocer el sindrome que presenta, se comienza un tratamiento de fisioterapia, en el que se tienen en cuenta las caracteristicas del sindrome. Se trabaja el alineamiento corporal y la carga de peso en el hemicuerpo derecho, a traves de actividades significativas para ella. Resultados Se evidencia eficacia del tratamiento, utilizando 3 escalas que miden la gravedad del sindrome. Discusion Se concluye que hacen falta mas estudios para la comprension profunda de los mecanismos lesionales y la adaptacion del tratamiento. Conclusion Se evidencia la importancia del conocimiento de las caracteristicas del sindrome por parte del fisioterapeuta y del equipo de atencion directa, asi como de la familia, para realizar un tratamiento eficaz.

Most teratomas involving the thyroid gland are benign and occur in children. However, the adult cases reported are mostly malignant. Many of the cases previously described in the medical literature have fatal outcome because of spread of the tumor refractory to treatment. We report a case of primary malignant teratoma of the thyroid in a 38-year-old pregnant black woman. She was treated with a combination of surgery, and postoperative chemotherapy with good initial response.

Summary: Light microscope and ultrastructural studies of normal infants and children testes revealed the presence of primary spermatocytes and occasional spermatids at 4, 8, 9, 11, 12 and 13 years of age, but not in all the boys of these ages. When they were found they appeared in both testes, but only in a 5–25% of the seminiferous tubules. These spermatocytes undergo degeneration or progress to abnormal spermatids which degenerate in turn. Spermatozoa were never found. Zusammenfassung: Das Auftreten primarer Spermatozyten in den Hoden von Kindern und Kleinkindern Lichtmikroskopische und ultrastrukturelle Untersuchungen der Hoden normaler Kinder und Kleinkinder wiesen das Vorhandensein primarer Spermatozyten und gelegentlich Spermatiden im Alter von 4, 8, 9, 11, 12 und 13 Jahren nach, jedoch nicht bei alien Jungen der genannten Altersgruppen. Wenn diese Zellen nachgewiesen werden konnten, waren sie in beiden Hoden vorhanden, aber nur in 5–25% der Tubuli seminiferi. Diese Spermatozyten unterliegen einer Ruckbildung oder einer Umwandlung in abnorme Spermatiden, die sich in der Folge zuruckbilden. Spermatozoen warden nie gefunden.

Two brothers have spermiograms with a similar pattern: absolute teratozoospermia with round-headed spermatozoa. The familial trait only has been previously one time in the literature. The spermatozoa show several abnormalities in the head. They lack acrosome and postacrosomal sheath. The nuclei are small and the chromatin is distributed in small groups. The nuclear envelope has abundant pores and is loosely attached to the chromatin. All the nuclei have brown inclusions, refringent when they are observed under the light microscope, vesicular and laminar under the electron microscope. Other abnormalities less frequently observed are: irregularities in the mitochondrial sheath, loss of parallelism of the dense fibres and duplication and angulation of the sperm tail. The hormonal assays and the biochemical tests are normal in both patients.

Resumen Objetivo Estabilizar el saco aneurismatico y evitar la formacion de fugas tipo II en el tratamiento endovascular de los aneurismas de aorta abdominal (AAA), creando experimentalmente un modelo animal y tratandolo mediante la colocacion de endoprotesis y la ocupacion del saco aneurismatico. Material y metodos Se crearon AAA de forma experimental en cerdos y en ovejas. Se trataron con protesis endovasculares y se estabilizaron, en el mismo procedimiento, introduciendo ethibloc y onix a traves de un cateter vascular situado dentro del saco aneurismatico. En todos se realizaron controles con aortografia y, de forma aleatoria, con angiorresonancia magnetica y tomografia computarizada abdominal. Se efectuaron estudios macroscopicos e histopatologicos. Se analizaron 2 ovejas 1 ano despues. Se valoraron las caracteristicas de los materiales empleados, su difusion en las arterias colaterales y su eficacia para rellenar el saco del aneurisma. Resultados En todos los animales se consiguio, con exito, la realizacion del procedimiento. La supervivencia de los cerdos fue del 100 %, mientras que de una mayor labilidad de las ovejas para la anestesia, resulto una mortalidad perioperatoria del 50 %. De los materiales empleados, tanto ethibloc como onix son faciles de utilizar y resultan estables con el paso del tiempo. Conclusion Es posible rellenar el saco de un AAA tratado con endoprotesis y sus colaterales, en el mismo procedimiento, con materiales introducidos a traves de un cateter.

TWIST1 is a basic helix–loop–helix (bHLH) transcription factor that has been involved in tumor progression and metastasis in several cancer types, although no evidence has been provided yet on its implication in colorectal carcinogenesis. We examined the expression pattern of TWIST1 messenger RNA (mRNA) in 54 colorectal cancer biopsies compared with each respective adjacent normal mucosa by real-time reverse-transcriptase polymerase chain reaction (RT-PCR) methodology. TWIST1 mRNA was found significantly overexpressed in colorectal cancer samples compared to nontumorous colon mucosa (P

Colorectal adenocarcinoma is the second cause of cancer mortality in developed countries. Rac1 is a member of the family of Rho GTPases that regulates many intracellular signaling pathways, including those involved in tumorigenesis, invasion, and metastasis. We have investigated the role of Rac1 in colorectal tumor progression by genetic modification of the human colorectal adenocarcinoma cell line SW620 to either overexpress Rac1 or lack Rac1 expression. Tumor behavior was studied by orthotopic injection of stably modified cell lines into the cecal wall of athymic nude mice, a model that replicates the histopathological appearance and clinical behavior of human colorectal adenocarcinoma in humans. While overexpression of Rac1 resulted in an accelerated tumorigenic process, inducing a faster mortality rate, inhibition of Rac1 completely suppressed tumor formation. These results suggest that Rac1 plays a major role in colorectal adenocarcinoma progression. Finally, interference with Rac1 function may provide an important tool to block the malignant phenotype of colorectal adenocarcinoma cells.

Summary Background Adequate prognostic markers to predict outcome of patients with lung cancer are still needed. The aim of this study was to assess whether choline kinase alpha (ChoKα) gene expression could identify patients with different prognoses. ChoKα is an enzyme involved in cell metabolism and proliferation and has a role in oncogene-mediated transformation in several human tumours, including lung cancer. Methods 60 patients with non-small-cell lung cancer (NSCLC) who had undergone surgical resection in a single centre were enrolled into the study as the training group. We used real-time reverse-transcriptase PCR (RT-PCR) to measure ChoKα gene expression and analyse the association between ChoKα expression and survival in evaluable patients. Additionally, a second group of 120 patients with NSCLC from a different hospital were enrolled into the study as the validation group. We did an overall analysis of all 167 patients who had available tissue to confirm the cut-off point for future studies. The primary endpoints were lung-cancer-specific survival and relapse-free survival. Findings Seven of the 60 patients in the training group were not evaluable due to insufficient tissue. In the 53 evaluable patients, the cut-off for those with ChoKα overexpression was defined by receiver operator under the curve (ROC) methodology. 4-year lung-cancer-specific survival was 54·43% (95% CI 28·24–80·61) for 25 patients with ChoKα expression above the ROC-defined cut-off compared with 88·27% (75·79–100) for 28 patients with concentrations of the enzyme below this cut-off (hazard ratio [HR] 3·14 [0·83–11·88], p=0·07). In the validation group, six of the 120 enrolled patients were not evaluable due to insufficient tissue. For the other 114 patients, 4-year lung-cancer-specific survival was 46·66% (32·67–59·65) for those with ChoKα expression above the ROC-defined cut-off compared with 67·01% (50·92–81·11) for patients with concentrations of ChoKα below the cut-off (HR 1·87 [1·01–3·46], p=0·04). A global analysis of all 167 patients further confirmed the association between ChoKα overexpression and worse clinical outcome of patients with NSCLC: 4-year lung-cancer-specific survival for ChoKα expression above the ROC-defined cut-off was 49·00% (36·61–60·38) compared with 70·52% (59·80–76·75) for those with concentrations of ChoKα below the cut-off (HR 1·98 [1·14–3·45], p=0·01). The overall analysis confirmed the cut-off for ChoKα expression should be 1·91-times higher than concentrations noted in healthy tissues when ChoKα is used as an independent predictive factor of relapse-free and lung-cancer-specific survival in patients with early-stage NSCLC. Interpretation ChoKα expression is a new prognostic factor that could be used to help identify patients with early-stage NSCLC who might be at high risk of recurrence, and to identify patients with favourable prognosis who could receive less aggressive treatment options or avoid adjuvant systemic treatment. New treatments that inhibit ChoKα expression or activity in patients with lung cancer should be studied further.

Non-small-cell lung cancer (NSCLC) represents the most frequent and therapy-refractive sub-class of lung cancer. Improving apoptosis induction in NSCLC represents a logical way forward in treating this tumor. Cisplatin, a commonly used therapeutic agent in NSCLC, induces activation of N-terminal-c-Jun kinase (JNK) that, in turn, mediates induction of apoptosis. In analysing surgical tissue samples of NSCLC, we found that expression of MKP1/CL100, a negative regulator of JNK, showed a strong nuclear staining for tumor cells, whereas, in normal bronchial epithelia, MKP1 was localized in the cytoplasm as well as in nuclei. In the NSCLC-derived cell lines H-460 and H-23, we found that MKP1 was constitutively expressed. Expressing a small-interfering RNA (siRNA) vector for MKP1 in H-460 cells resulted in a more efficient activation by cisplatin of JNK and p38 than in the parental cells, and this correlated with a 10-fold increase in sensitivity to cisplatin. A similar response was also observed in H-460 and H-23 cells when treated with the MKP1 expression inhibitor RO-31-8220. Moreover, expression of a siRNA-MKP2, an MKP1-related phosphatase, had no effect on H-460 cell viability response to cisplatin. Tumors induced by H-460 cells expressing MKP1 siRNA grew slower in nu-/nu- mice and showed more susceptibility to cisplatin than parental cells, and resulted in an impaired growth of the tumor in mice. On the other hand, overexpression of MKP1 in the H-1299 NSCLC-derived cell line resulted in further resistance to cisplatin. Overall, the results showed that inhibition of MKP1 expression contributes to a slow down in cell growth in mice and an increase of cisplatin-induced cell death in NSCLC. As such, MKP1 can be an attractive target in sensitizing cells to cisplatin to increase the effectiveness of the drug in treating NSCLC. © 2006 Nature Publishing Group All rights reserved., This work was supported by the following grants: no. 08.1/0048.1/2003 from the Comunidad Autónoma de Madrid; no. 01/1094, no. 02/0774 and no. 02/1094 from the Fondo de Investigación Sanitaria; no. RTICC C03/10 from Instituto de Salud Carlos III. The investigators RM-P and CM-G are supported by Grant no. RTICC C03/10.

El macroorquidismo es una entidad poco frecuente en niños y que suele aparecer formando parte del síndrome X frágil. Otras posibles etiologías son el hipotiroidismo primario de larga evolución, los restos adrenales en la hiperplasia suprarrenal congénita, los macroadenomas secretores de hormona foliculoestimulante (FSH), los tumores locales, los linfomas o el déficit de aromatasa. En adultos el macroorquidismo bilateral puede constituir una variante de la normalidad. Presentamos el caso de un niño de 11,5 años remitido a nuestro hospital por haber presentado en los últimos meses un llamativo aumento bilateral del tamaño testicular. En la exploración física se objetivó un volumen testicular mayor de 30 ml. Las pruebas complementarias realizadas permitieron descartar las entidades hasta ahora descritas como causantes de macroorquidismo. Por tanto, se estableció el diagnóstico de macroorquidismo idiopático. La hiperplasia de células de Sertoli hallada en la biopsia testicular, sin existir concentraciones plasmáticas elevadas de FSH, induce a especular sobre una hipotética hiperfunción del receptor de la FSH como responsable del exagerado crecimiento testicular que este paciente presentaba. : Macroorchidism is a rare condition in children and is usually associated with fragile X syndrome. Other possible etiologies of macroorchidism are long-standing primary hypothyroidism, adrenal remnants in congenital adrenal hyperplasia, follicle stimulating hormone (FSH)-secreting pituitary macroadenomas, local tumors, lymphomas, and aromatase deficiency. Bilateral macroorchidism can be a normal variant in adult men. We report the case of an 11.5-year-old boy who was referred to our hospital for evaluation of marked bilateral testicular enlargement in the previous few months. Physical examination revealed a testicular volume larger than 30 ml. Complementary investigations allowed us to rule out all hitherto reported etiologies of bilateral macroorchidism and therefore a diagnosis of idiopathic macroorchidism was established. The increased number of Sertoli cells found on biopsy, without elevated plasma FSH levels, prompted us to speculate about a hypothetical FSH receptor hyperfunction as a possible cause of the exaggerated testicular enlargement in this patient.

Ghrelin, the endogenous ligand for the GH secretagogue receptor (GHS-R), has been primarily linked to the central neuroendocrine regulation of GH secretion and food intake, although additional peripheral actions of ghrelin have also been reported. In this context, the expression of ghrelin and its cognate receptor has been recently demonstrated in rat testis, suggesting a role for this molecule in the direct control of male gonadal function. However, whether this signaling system is present in human testis remains largely unexplored. In this study we report the expression and cellular location of ghrelin and its functional receptor, the type 1a GHS-R, in adult human testis. In addition, evaluation of ghrelin and GHS-R1a immunoreactivity in testicular tumors and dysgenetic tissue is presented. The expression of the mRNAs encoding ghrelin and GHS-R1a was demonstrated in human testis specimens by RT-PCR, followed by direct sequencing. In normal testis, ghrelin immunostaining was demonstrated in interstitial Leydig cells and, at lower intensity, in Sertoli cells within the seminiferous tubules. In contrast, ghrelin was not detected in germ cells at any stage of spermatogenesis. The cognate ghrelin receptor showed a wider pattern of cellular distribution, with detectable GHS-R1a protein in germ cells, mainly in pachytene spermatocytes, as well as in somatic Sertoli and Leydig cells. Ghrelin immunoreactivity was absent in poorly differentiated Leydig cell tumor, which retained the expression of GHS-R1a peptide. In contrast, highly differentiated Leydig cell tumors expressed both the ligand and the receptor. The expression of ghrelin and GHS-R1a was also detected in dysgenetic Sertoli cell-only seminiferous tubules, whereas germ cell tumors (seminoma and embryonal carcinoma) were negative for ghrelin and were weakly positive for GHS-R1a. In conclusion, our results demonstrate that ghrelin and the type 1a GHS-R are expressed in adult human testis and testicular tumors. Overall, the expression of ghrelin and its functional receptor in human and rat testis, with roughly similar patterns of cellular distribution, is highly suggestive of a conserved role for this newly discovered molecule in the regulation of mammalian testicular function.

EVIDENCE FOR AUTOSOMAL DOMINANT INHERITANCE THROUGH THE MATERNAL LINE IN A CASE OF PRIMARY CILIARY DISKINESIA. An atypical case of primary ciliary dyskinesia is presented in which the inheritance, rather than the classical autosomal recessive, appears to be transmitted as an autosomal dominant trait through the maternal line. The case involves two brothers of 29 and 30 years of age, married without children, with a history of infertility, frequent episodes of sinusitis, and recurrent pulmonary infections. Their mother and sister have chronic bronchopathy of unknown etiology. Their father is healthy without pulmonary problems or sinusitis. At physical exam, both brothers, sister and mother presented with bronchial rhonchi at lung auscultation. Blood analysis and pulmonary function, liver and renal tests were all normal. The ultraestructual study of the sperm flagellum by electron microscopy revealed that both brothers have the same anomaly. Namely, in the majority of the cross-sections, both dynein arms are missing. The nexin filament was present, as well as the radial spokes and the central pair of microtubules. In some sperm, besides the absence of dynein arms, there was also absence of the central pair of microtubules. Neither anomalies of the fibrous sheath nor of the dense fibers were found. In approximately 50% of the spermatozoa, the midpiece had a decreased number of mitochondria and extra non- aligned mitochondria. Other findings included extra peripheral microtubules in the axoneme.

The gonadal biopsy provides essential information for the identification, classification and early detection of neoplasias in patients with disorders of sex development. Histopathological findings in these cases must be analysed together with clinical, hormonal, genetic and molecular information before deciding a therapeutic option. Sexual differentiation is the result of multiple and complex genetic and endocrinal mechanisms; therefore, we first present the events taking place during gonadal embryonic development, focusing on the genetic mechanisms involved in sexual determination and the differentiation of the testis and the urogenital tract. In second place, we describe the different gonads in the intersexual states -in testicular regression syndrome, fibrous streak, testicular dysgenesis, streak testes, ovotestes and microscopically normal testes and ovaries-, highlighting the histological features and the differential findings that allow the pathologist to distinguish between these entities with the aid of clinical, genetic, hormonal and molecular information that are characteristic for each situation. In third place, we studied the incidence of neoplasias in gonadal dysgenesis, male pseudohermaphroditism and true hermaphroditism. Finally, we discuss the limitations of gonadal biopsy to achieve a correct diagnosis in the disorders of sex development.

We present the case of a newborn with sternal cleft (SC) and presternal enterogenous cyst operated on during the neonatal period. SC is an uncommon congenital malformation of the thoracic wall which can occur as an isolated form or in association with other malformations. To our knowledge, the presence of SC and enterogenous cyst has not been described to date. Early surgical repair of SC gives good aesthetic and functional results and is usually the preferred approach.

To create an animal model to stabilize the aneurysmal sac and prevent type II leaks in the endovascular treatment of aneurysms of the abdominal aorta (AAA) by placing an endoprosthesis (stent-graft) and filling the aneurysmal sac.AAA were experimentally induced in pigs and sheep; AAA were subsequently treated with endovascular stent grafts and stabilized in the same procedure by introducing ethibloc and onyx through a vascular catheter placed within the aneurysmal sac. All animals underwent aortography, and MR angiography and abdominal CT were performed on randomly selected animals. Histological studies included both macroscopic and microscopic examination. Two sheep were analyzed one year after the procedure. We evaluated the characteristics of the materials employed, their diffusion in the collateral arteries, and their efficacy in stabilizing the aneurysmal sac.The procedure was successfully carried out in all animals. Survival in the pigs was 100 %, whereas greater instability under anesthesia in the sheep led to 50 % perioperative mortality. Both ethibloc and onyx were considered easy to use and stable over time.The sac of an AAA treated with an endovascular stent graft and its collateral vessels can be treated in the same procedure with materials introduced through a catheter.

Myofibroblastic inflammatory tumor is a controversial entity that shows great variability in clinical presentation, histological findings, evolution, and prognosis. It is a rare cause of primary lung tumor in adults; however, it is the most common cause of lung tumors in children. The diagnosis is fundamentally histological, although histological diagnosis is not easy because myofibroblastic inflammatory tumor is characterized by a polymorphic cellular infiltration of variable cellular composition that could be similar to other diseases such as lymphoma or low-grade sarcoma. We report the case of a 23-year-old woman in whom a solitary pulmonary nodule was discovered incidentally at plain-film chest x-ray.

An atypical case of primary ciliary dyskinesia is presented in which the inheritance, rather than the classical autosomal recessive, appears to be transmitted as an autosomal dominant trait through the maternal line. The case involves two brothers of 29 and 30 years of age, married without children, with a history of infertility, frequent episodes of sinusitis, and recurrent pulmonary infections. Their mother and sister have chronic bronchopathy of unknown etiology. Their father is healthy without pulmonary problems or sinusitis. At physical exam, both brothers, sister and mother presented with bronchial rhonchi at lung auscultation. Blood analysis and pulmonary function, liver and renal tests were all normal. The ultraestructual study of the sperm flagellum by electron microscopy revealed that both brothers have the same anomaly. Namely, in the majority of the cross-sections, both dynein arms are missing. The nexin filament was present, as well as the radial spokes and the central pair of microtubules. In some sperm, besides the absence of dynein arms, there was also absence of the central pair of microtubules. Neither anomalies of the fibrous sheath nor of the dense fibers were found. In approximately 50% of the spermatozoa, the midpiece had a decreased number of mitochondria and extra non-aligned mitochondria. Other findings included extra peripheral microtubules in the axoneme.

Macroorchidism is a rare condition in children and is usually associated with fragile X syndrome. Other possible etiologies of macroorchidism are long-standing primary hypothyroidism, adrenal remnants in congenital adrenal hyperplasia, follicle stimulating hormone (FSH)-secreting pituitary macroadenomas, local tumors, lymphomas, and aromatase deficiency. Bilateral macroorchidism can be a normal variant in adult men. We report the case of an 11.5-year-old boy who was referred to our hospital for evaluation of marked bilateral testicular enlargement in the previous few months. Physical examination revealed a testicular volume larger than 30 ml. Complementary investigations allowed us to rule out all hitherto reported etiologies of bilateral macroorchidism and therefore a diagnosis of idiopathic macroorchidism was established. The increased number of Sertoli cells found on biopsy, without elevated plasma FSH levels, prompted us to speculate about a hypothetical FSH receptor hyperfunction as a possible cause of the exaggerated testicular enlargement in this patient.

Thoracic duct cyst presenting as an hour-glass shaped mass in the left supraclavicular area: case report. Thoracic duct cysts are a very rare entity in the head and neck pathology. We present a case of a 52 year-old man, who was referred to our service, complaining by a 30 days left cervical mass, with no other symptoms. A 6 cm cystic mass was revealed after ultrasonography and CT. Needle aspiration confirmed the presence of lymph in the cyst. The treatment was simple excision. Special care was taken to ligate the connected lymphatic vessels.

To describe for the first time a lesion termed lipomembranous fat necrosis (LFN) in three patients with spermatic cord torsion.We reviewed 386 testes and their epididymides and spermatic cords which had been removed for testicular infarction. For the three cases showing LFN, a battery of histochemical tests (including periodic acid-Schiff (PAS), orcein, Sudan black and Perls stains) was applied and clinical histories and laboratory data were also investigated. Findings were similar in the three specimens. The testes showed a central group of necrotic seminiferous tubules which were surrounded by granulation tissue consisting of macrophages, multinucleated giant cells, lymphocytes, plasma cells and fibrous connective tissue at the periphery of the lesion. The spermatic cord showed thrombosed veins surrounded by fat necrosis showing cystic cavities which were bounded by wavy hyaline membranes. These stained with Sudan black, PAS (before and after diastase digestion) and orcein and presented yellowish-green autofluorescence.Lipomembranous fat necrosis of the spermatic cord is a distinctive entity which seems to be related to spermatic cord torsion and the differential diagnosis of which should be established with regard to the presence of parasites, sclerosing lipogranuloma and granuloma evoked by rupture of a testicular prosthesis.

Despite the knowledge and histological classification of testicular lesions, epididymal lesions associated with cryptorchidism are not well defined and only macroscopic alterations have been reported. We have evaluated the alterations in the growth of both the epithelium and muscular wall of efferent ducts and epididymis in human patients with cryptorchidism from infancy to adulthood. In addition, by cytokeratin immunostaining we have also evaluated the stage of differentiation of each segment along the human postnatal life in these patients. A decrease is shown in the size of efferent and epididymal ducts in cryptorchid children compared with normal, age-matched controls. The height of the epithelium, muscular wall, and lumen of the cryptorchid epididymis were reduced at every age studied. This decrease in all regions was seen even in the testicular quiescent period (1 to 4 years of age). In addition, the cryptorchid epididymis grows more slowly during the transition to the pubertal period. The smaller size of the cryptorchid epididymis in pubertal and adult men compared with that of normal men is due primarily to underdevelopment of the muscular wall and a reduction in epithelial height. The pattern of growth of cryptorchid efferent ducts and ductus epididymides parallels that in normal men, except that development of the lumen and muscular layer in the cauda epididymis region are delayed. Epithelial differentiation, monitored by cytokeratin expression, is minimal in efferent ducts and throughout the epididymis of the cryptorchid male, and this is already seen in children. In conclusion, our immunohistochemical and morphometric results show a reduced development of the human cryptorchid epididymis that is already evident in childhood. They indicate that cryptorchidism is a primary congenital illness of the testis and spermatic ducts, with evident lesions from the first years of life, and suggest that surgical descent would probably not be able to completely reverse these alterations.

Androgen receptor (AR) immunohistochemistry was performed in an archival collection of adult human cryptorchid testes to determine whether AR cellular distribution and intensity of immunostaining were functions of the severity of cellular dysgenesis. The seminiferous tubule histology of cryptorchid testes collected from adults is marked by three specific patterns. 1) Seminiferous tubules are characterized as maintaining focal areas of germinal cell differentiation (albeit incomplete) that are interspersed with 2) tubules composed of Sertoli cells only, these latter cells being principally of the adult type, although dysgenetic and immature Sertoli cells may also be detected. 3) In contrast, there is a class of tubule that is characterized as being composed exclusively of Sertoli cells that are extremely dysgenetic in appearance. The majority of adult-type Sertoli cells found in the first types of tubules exhibited either robust or moderate AR staining intensity. Peritubular cells of these tubules also expressed a similar AR staining intensity. In contrast, in the more dysgenetic and immature type Sertoli cells found in the second type of tubules, the intensity of AR staining was significantly less, if not missing altogether. Finally, in the most dysgenetic tubules, Sertoli cell AR staining was never detected. To our knowledge, this is the first report in the literature that addresses the intensity of AR immunostaining in Sertoli cells of cryptorchid testes. The results presented herein are consistent with the interpretation that the intensity of AR staining in Sertoli cells diminishes as a function of the severity to which the cells are afflicted within a cryptorchid testis and that focal absence of AR expression in Sertoli cells correlates with a lack of local spermatogenesis in the tubules.

To report a case of locally invasive angiomyofibroblastoma of the scrotum. To our knowledge, this is the first case of invasive scrotal angiomyofibroblastoma reported in the literature.A case of invasive angiomyofibroblastoma of the scrotum is presented. The literature is reviewed with special reference to the etiopathogenesis, clinical features, diagnosis and treatment of this rare soft tissue tumor.The case described herein shows that angiomyofibroblastoma can be invasive.

Biopsy of the testis is not universally accepted in contrast with biopsies of other organs. The pathologist studies and reports on the pathophysiology of the testicular biopsy specimen. Methodology requires the inclusion of qualitative and quantitative studies, the evaluation of the lesion's evolution (prognosis), and, often, therapeutic advice regarding treatment. Cooperation between pathologists and clinicians optimizes the utility of the biopsy for the patient.

Hyalinizing trabecular adenoma (HTA) is a follicle-derived tumor of the thyroid gland that has been described recently. The differential diagnosis includes medullar carcinoma, papillary carcinoma, and paraganglioma of the thyroid. We report a case of thyroid HTA in a 25-year-old woman. The tumor appeared as acold noduleof the left thyroid in radionuclide scans. Histologically, the tumor showed tumor cells arranged in trabeculae and a prominent hyaline stroma. The neoplastic cells were focally immunoreactive for thyroglobulin and negative for calcitonin, chromogranin, and S-100 protein. Three years after hemithyroidectomy, the patient is alive and free of disease.

To evaluate the morphometric, immunohistochemical, and ultrastructural lesions of the testes in prepubertal and adult patients with androgen insensitivity syndrome.We examined the testicular biopsy using immunohistochemistry for vimentin, smooth muscle actin, and collagen IV antigens. Quantification of seminiferous tubules and testicular interstitium was performed in prepubertal and adult patients with androgen insensitivity syndrome and results were compared with normal testes from both infants and adults.The adult testes presented nodular and diffuse lesions that consisted of Sertoli-cell-only seminiferous tubules. Two types of Sertoli cells could be distinguished, namely, immature vimentin-positive Sertoli cells and nearly mature Sertoli cells. In the nodules, the lamina propria was thin and contained a scant number of actin-positive peritubular cells. Leydig cells were hyperplastic. The prepubertal patients showed only diffuse lesions characterized by Sertoli cell hyperplasia, decreased germ cell numbers, and a discontinuous immunoreaction to collagen IV.The testicular lesions in androgen insensitivity syndrome are probably caused by primary alterations that begin during gestation. These lesions become progressively more pronounced at puberty, when the nodular lesion pattern (adenomas) is completely developed.

The immunohistochemical reaction to oncostatin M (OSM) was studied in normal human testes at different ages (fetuses, newborns, children, pubertal boys, adults, and elderly men), as well as in several testicular disorders including carcinoma-in-situ cells (CIS), germ cell tumors, benign functioning Leydig cell tumor, androgen insensitivity syndrome, Klinefelter's syndrome, and cryptorchidism. Positive OSM immunostained Sertoli cells were only observed in fetuses. In normal testes, intense OSM immunoreaction was found in the Leydig cells of fetuses, newborns, and adults. Leydig cell immunoreaction was weak in elderly men and absent in children and pubertal boys. In some testicular disorders (Leydig cell tumor, cryptorchidism, and CIS), Leydig cell immunoreaction was as intense as in normal adult testes. This immunoreaction was heterogeneous in androgen insensitivity syndrome and was absent in Klinefelter's syndrome and intratubular seminoma. No recognizable Leydig cells were observed in the other testicular tumors. The findings of our study suggest that, in humans, the down-regulation of OSM immunoexpression in Sertoli cells occurs early, and that OSM immunoreaction in the Leydig cells is associated with functionally active and differentiated Leydig cells.

Bilateral testicular biopsies and clinical histories from 34 adult men with maturational arrest of spermatogonia were examined. According to the morphology of Sertoli cell nuclei, five testicular types of spermatogonial maturational arrest were established. In type I lesion, Sertoli cells resembled the immature Sertoli cells of infant testes. These cells had a round, regularly outlined, dark nucleus with a small nucleolus. The seminiferous tubules showed no apparent lumen and a poorly developed lamina propria lacking in elastic fibres. This lesion was found in patients exhibiting a eunuchoid phenotype, with small tests and low serum levels of gonadotrophins and testosterone (hypogonadotrophic hypogonadism). Type II lesion showed morphologically normal, mature, adult Sertoli cells which had a pale, irregularly outlined nucleus, many often triangle-shaped, with a large, centrally located nucleolus. The seminiferous tubules were reduced in diameter and showed a few spermatocytes and spermatids. This lesion was found in patients with varicocoele, epididymitis, testicular trauma or idiopathic infertility. Serum FSH levels were normal or increased while LH and testosterone levels were normal. In type III lesion, Sertoli cells resembled the involuting Sertoli cells found in the testes of aging men, and displayed very infolded nuclei, with abundant dense chromatin patches and a large nucleolus. The seminiferous tubules showed a slightly dilated lumen and a normal tubular wall. The most relevant clinical findings in patients with this lesion were alcoholism, varicocoele, falciform cell anaemia, epididymitis and germ cell tumour. Serum follicle stimulating hormone (FSH) levels were normal or increased while luteinizing hormone (LH) and testosterone levels were normal. Type IV lesion Sertoli cells presented with a de-differentiated appearance. These cells had a small, round euchromatic nucleus with a small nucleolus and vacuolated cytoplasm. The seminiferous tubules were devoid of lumen or ectatic, and the tubular wall was thick and contained abundant elastic fibres. This lesion was characteristic of patients who underwent hormonal treatment because of prostatic carcinoma or sex change. Type V lesion showed abnormally differentiated, probably dysgenetic, Sertoli cells which had a round to ovoid regularly outlined nucleus, with small heterochromatin granules, and the number of these cells was increased. The seminiferous tubules had a central lumen, or were ectatic with vacuolated Sertoli cells, and the amount of elastic fibres was decreased. The most relevant clinical finding in patients with this lesion was orchidopexy. Serum FSH and LH levels were normal or slightly increased. These findings indicate that spermatogonial maturational arrest is associated with a characteristic Sertoli cell morphology that can be easily identified. This morphology may shed light on the aetiology of the disorder, and be useful for establishing the prognosis and bases for treatment in subfertile patients.

The distribution of the androgen receptor (AR) in archival human testes was determined immunocytochemically using an affinity-purified peptide-specific rabbit antibody, PG21, and employing a modified biotin-streptavidin-immunoperoxidase method that incorporated a biotin amplification step. In combination with microwave epitope retrieval, the biotin amplification step increased the sensitivity of the immunostaining assay approximately 20-fold. Thus, the useful range at which PG21 rendered a robust, specific immunostaining signal without also increasing nonspecific background was extended dramatically. Broadening the useful range of the PG21 antibody made it possible to resolve the relative amounts of immunopositive AR in different cell types of the human testis. At a high PG21 concentration, for example, all AR-positive cells exhibited a robust immunostaining intensity, but it was not possible to distinguish between nuclei exhibiting either high or moderate immunostaining intensities. In contrast, as the concentration of PG21 was decreased, distinct populations of testicular cells exhibited differential AR immunostaining intensities in their nuclei. AR immunostaining of Sertoli cell nuclei was present at low PG21 concentrations at which no immunostaining of peritubular myoid cells or Leydig cells could be detected. In turn, AR immunostaining of peritubular myoid cells was detected at PG21 concentrations that did not immunostain Leydig cells. Moreover, within the seminiferous epithelium, Sertoli cell nuclear AR staining intensity was less at stages V and VI of the cycle of the seminiferous epithelium than that at stage III, and stage III staining intensity was greater than that at stages I and II. This AR immunostaining pattern in human Sertoli cell nuclei as a function of the cycle of the seminiferous epithelium is reminiscent of the pattern observed in rodent species. Finally, no AR immunostaining of germ cells was observed at any of the PG21 concentrations examined.

Among the different techniques used to detect oncogene amplification in tumor DNA, Southern blot and differential PCR have been the most frequently used. We report on a technical comparison of three different methods to detect gene amplification by differential PCR: ethidium bromide staining, silver staining (both after standard differential PCR), and fluorescent differential PCR. We explored the relative densitometric measure of a 119 bp fragment of the CDK4 gene versus an 82 bp fragment of the IFNG gene. In total agreement with previous studies carried out by Southern blot and differential PCR by other authors, we were able to detect CDK4 amplification in 3 of the 21 glioblastomas (14%), but only by the fluorescent differential PCR method. In conclusion, fluorescent differential PCR is more sensitive than standard differential PCR for detection oncogene amplification in tumor DNAs.

To evaluate the status of the intratesticular spermatic duct system (rete testis, RT) in patients with cryptorchidism.We examined 40 surgical orchiectomy specimens from postpubertal patients with undescended testis from pathology files at La Paz Hospital, Madrid, Spain. Special attention was given to the intratesticular spermatic duct system, mainly the RT.In all cases, the RT was underdeveloped and was lined by columnar or large cuboidal cells (dysgenetic RT). According to the configuration of the mediastinal RT, the lesions were classified as diffuse hypoplastic RT (37.5%), hypoplastic-cystic RT (50%), or adenomatous pseudohyperplastic RT (12.5%).Although these changes could have resulted from incomplete pubertal maturation, many other data suggest that a primary abnormality of the RT is present. Important clinical considerations are derived from the fact that a functional obstruction of the sperm-conducting mechanism is determined by these abnormalities of the RT. The presence of intraluminal spermatozoa in epididymis and RT suggest that at least some of these patients are potentially fertile.

In a histologic review of adult epididymides obtained at autopsy (both epididymides of 408 men) or during surgery (261 men with testicular or epididymal nontumoral pathology), a peculiar granulomatous lesion was observed in two autopsy specimens (unilateral) and three surgical specimens. The lesion was located in the caput epididymidis and consisted of a zone of necrosis that involved efferent ducts and interstitial connective tissue and was not associated with an acute inflammatory response. Immunohistochemical study with anticytokeratin antibodies showed the presence of some epithelial cells in the damaged efferent ducts. At the periphery of the lesion, where damage was less severe, the efferent ducts only showed partial necrosis of their wall through which the necrotic material was released to the ductal lumen. Inflammatory infiltrates were scanty and consisted of lymphocytes and CD68-positive macrophages. Lymphocytes were mainly located around the necrotic zone or surrounding the adjacent, well-preserved efferent ducts, whereas macrophages formed large clusters in the ductal lumen. In these clusters, cholesterol crystals and giant cells of foreign body type were frequent. Intratubular epithelial regeneration as well as proliferation of small ducts showing epithelial regeneration and numerous spermatozoa in their lumen were observed. Ceroid granulomata, spermatic granulomata, and epidermoid metaplasia of the efferent ducts were observed in some cases. On the basis of the histologic study, the following developmental stages of the lesion are suggested: ischemic necrosis, granulomatous reaction, cicatrization, and sequelae. The term "granulomatous ischemic lesion" is proposed to designate this reactive lesion.

Adrenocortical tumors are uncommon in childhood. The incidence of these tumors is about 0.3-0.4% of all the solid tumors in childhood. Because of its low incidence, there are no established protocols or uniform histological classification. Most of these endocrine tumors are hormone producing, causing virilization, Cushing's syndrome, feminization, hiperaldosteronism or hipoglicemy. Only a few of these do not produce hormones. The treatment is always surgical. The efficacy of another treatments (chemotherapy or radiotherapy) has not been demonstrated in infancy. It prognosis depends on the age and the resectability.

We describe a 12-year-old patient with a primary pulmonary mass in the left upper lung. The diagnosis of inflammatory pseudotumour was suspected preoperatively. After pathological examination and complete clinical evaluation, a diagnosis of malignant primary pulmonary fibrous histiocytoma was established. This is a very uncommon primary neoplasm of the lung and to our knowledge only five paediatric cases have been reported. Because of the rarity of these sarcomas and histological similarities to benign inflammatory pseudotumour, care must be taken to avoid confusion between the two disorders particularly in intra-operative frozen sections.Primary malignant fibrous histiocytoma of the lung is an uncommon tumour that should be considered in the differential diagnosis of pulmonary neoplasms of childhood. The histological diagnosis can be difficult due to the similarities with inflammatory pseudotumour.

Coronary fibrinolysis through intravenous via is a usual technique in ICU worldwide, it is a procedure of controlled risk which provides great benefits to patients who undergo such technique. The role of nursing in the administration and control of the fibrinolytic treatment is essential. Despite that, the plans for fibrinolysis specific care are very scarce, if not inexistent, in the bibliography reviewed. The main objective of this work is identify the complications derived from the administration of fibrinolytic medicines through intravenous via. Using a chart of collected data, which goes from the admission of the patient to their discharge from ICU, 178 cases are studied. After the analysis of results, a standardization of intensive care units orientated to increase the assistance quality is suggested.

Five cases of large cell calcifying Sertoli cell tumour of the testis not associated with complex dysplastic syndromes are reported. The age of the patients ranged from 13 to 34 years and all the tumours were histologically similar, having large, isomorphic, non-mitotic, eosinophilic Sertoli cells with foci of calcification. Flow cytometry demonstrated the cells to be diploid or hypodiploid. All cases were positive for vimentin and focally positive for low molecular weight keratin. The present cases, together with a review of the 22 previously reported tumours, demonstrate that there are two clear cut types of large cell calcifying Sertoli cell tumour; those which are associated with complex dysplastic syndromes and which are bilateral and multifocal, and those which are not associated and are unilateral and focal. Prognosis in all of our cases was uniformly good despite invasion of the rete testis in two cases. It is considered that conservative resection of the tumour is the treatment of choice in cases not associated with complex dysplastic syndromes, since the malignancy rate is low.

A high incidence of visceral leishmaniasis has been documented in HIV-infected patients in endemic areas. In these patients, atypical locations and a chronic course of the disease are more frequent. Two AIDS patients with laryngeal leishmaniasis are reported. These cases are believed to be the first of this type documented in the literature. The possible pathogenic mechanisms of the disease are discussed. Infection with Leishmania donovani may eventually be described for every organ containing phagocytic cells.

Macro-orchidism (MO) is the increase of the testicular volume, up to 25 ml in the adult male. It is frequently associated with mental retardation (MR) with fragile X-chromosome (FXC) (Martin-Bell syndrome). Sometimes it is of unknown origin and is called "benign idiopathic macro-orchidism" (BIMO). MO has also been described in association with bilateral testicular tumors, idiopathic precocious puberty, juvenile hypothyroidism and, more rarely, with congenital testicular cysts (cystic testicular dysplasia) and testicular microlithiasis in a patient treated with GH. The most common presentation is MR associated with MO, with positive or negative FXC. Among MO with MR and FXC-marfanoid habitus patients have been described and in the Atkin-Flaitz syndrome patients. Management of MO must be conservative in all cases and testicular biopsy must only be performed to diagnose leukemic infiltration or carcinoma in situ (CIS), or as the last fertility diagnostic test in BIMO. A wide range of primary testicular lesions may histopathologically be found: preserved spermatogenesis tubes, only Sertoli cell pattern and complete tubular sclerosis. Interstitial edema, frequently implicated in the MO pathogeny, does not explain by itself the important increase in testicular volume. In our laboratory, we have demonstrated that the increment of the testicular volume in MO is associated with a significant increase in the length of the seminiferous tubules. MO may pathogenically be intimately related to some hormonal regulation mechanism or to a higher seminiferous tubule sensitivity to FSH.

La granulomatosis broncocentrica es una reaccion granulomatosa necrosante centrada alrededor de los bronquios y bronquiolos. En pacientes asmaticos, se considera que la granulomatosis broncocentrica representa una reaccion de hipersensibilidad frente a antigenos fungicos intrabronquiales. Sin embargo, en pacientes sin asma todavia no se ha identificado el posible agente etiologico de esta lesion en el tracto respiratorio Presentamos el caso de una mujer de 46 anos con granulomatosis broncocentrica asociada a hidatidosis pulmonar. Los posibles mecanismos inmunopatogenicos desencadenantes de las lesiones bronquiales en este caso se discuten brevemente

An immunohistochemical and semiquantitative study of the apical mitochondria-rich cells (AMRC) in the caput, corpus and cauda of the human epididymis from the fetal period to adulthood was performed on autopsy specimens from normal males without testicular or associated pathology. The immunohistochemical pattern of AMRC differed from that of the principal cells (PC). AMRC showed a more intense immunoreaction to several keratin types (AE1 and AE3 keratin complexes, and keratins 18 and 19) and to oestradiol-related protein receptors than did PC. In addition, immunostaining with antibodies to epithelial membrane antigen was intense in PC and weak in AMRC. Two immunohistochemical types of basal cells were observed: one was similar to the AMRC and the other to PC. PC and AMRC were already present in fetuses of 24-27 wk gestation. Basal cells were only occasionally observed at this age, but became much more numerous in the 28-33 wk fetuses. No changes in the immunohistochemical patterns of any of these cell types were found during infancy and adulthood. The numbers of PC per unit length of basement membrane were very similar in the 3 epididymal regions and at all ages studied. In all age groups, the number of AMRC decreased from caput to cauda epididymis. In the caput and corpus, the number of AMRC rose during the fetal period and the first 6 months after birth and thereafter decreased progressively during infancy and adulthood.

Trabajo presentado al 21th Meeting of the European Association for Cancer Research celebrado en Bruselas (Belgica) del 25 de Junio al 30 de Junio de 2010.

e17502 Background: Cisplatin-based adjuvant chemotherapy improves survival among patients with completely resected non-small cell lung cancer. However, objective response rates are in the range of ...

Background Human spermatogenesis is regulated by activation of the nuclear androgen receptor (AR) of Sertoli cells. Aim AR expression has been examined in three congenital diseases with severely damaged testis and cryptorchidism (17 cases), androgen insensibility syndrome (AIS) (6 cases) and Klinefelter syndrome (9 cases). Methods Morphologic, immunohistochemical and morpho-metric evaluation, as well as PCR detection of the CAG-triplet of AR. Results In complete spermatogenesis most Sertoli cells show intense nuclear AR expression, with intensity variable from cell to cell, depending on the maturation stage of spermatogenesis, and it is completely absent in germ cells. In azoospermic human testis, AR expression in Sertoli cells is higher in number and intensity in Sertoli cell-only pattern than in those with spermatogenesis arrest, or as compared with normal testis (control group). In cryptorchidia, the tubules with disgenetic or immature Sertoli cells had no anti-AR antibody reactivity. These results suggest a direct correlation between AR expression decrease and severity of the cryptorchidic disgenetic lesions. Sertoli cells are highly disgenetic in Klinefelter syndrome and their nuclei show a variable AR-immunoexpression spectrum from moderately positive to completely negative nuclei. Conclusions AR-expression is not substantially modified in hypospermatogenic or in atrophic areas of seminiferous tubules. Testicular lesions in cryptorchidic patients, in AIS testis and in testicular biopsies of patients with Klinefelter syndrome are associated with AR immunoexpression alterations, although apparently these alterations are not due to AR important mutations, as we have not found abnormal bands of CAG-triplet of AR in cryptorchidism and AIS.

We describe an intratesticular mucinous cystadenocarcinoma in a 59-year-old man. The tumor was bilateral and appeared in the right testis and the left epididymis. The testicular tumor was a well-demarcated nodule, 3.5 cm in diameter, that extended from the lower testicular pole (close to the albuginea) to the epididymis compressing the corpus and infiltrating the cauda. The contralateral tumor, a 2.5-cm nodule located in the corpus epididymidis, compressed the ductus epididymidis. Both tumors consisted of multiple cavities varying in size, separated from one another by connective tissue septa that were incompletely lined by a columnar pseudostratified epithelium. The epithelial cells immunostained positively for carcinoembryonal antigen and comprised two cell types: cells showing a hyperchromatic nucleus, located in the basal portion of the cell, abundant rough endoplasmic reticulum, apical vacuoles, and numerous microvilli; and mucous cells. The cystic lumen showed a mucous content and sloughed epithelial cells. The differential diagnosis and histogenesis of these tumors is discussed.