RESUMEN
Objective: To investigate the clinical characteristics, treatments and fertility recovery of rudimentary horn pregnancy (RHP). Methods: The clinical data of 12 cases with RHP diagnosed and treated in Peking University Third Hospital from January 1, 2010 to December 31, 2022 were retrospectively analyzed. Clinical informations, diagnosis and treatments of RHP and the pregnancy status after surgery were analyzed. Results: The median age of 12 RHP patients was 29 years (range: 24-37 years). Eight cases of pregnancy in residual horn of uterus occurred in type â residual horn of uterus, 4 cases occurred in type â ¡ residual horn of uterus; among which 5 cases were misdiagnosed by ultrasound before surgery. All patients underwent excision of residual horn of uterus and affected salpingectomy. After surgery, 9 patients expected future pregnancy, and 3 cases of natural pregnancy, 2 cases of successful pregnancy through assisted reproductive technology. Four pregnancies resulted in live birth with cesarean section, and 1 case resulted in spontaneous abortion during the first trimester of pregnancy. No uterine rupture or ectopic pregnancy occurred in subsequent pregnancies. Conclusions: Ultrasonography could aid early diagnosis of RHP while misdiagnosis occurred in certain cases. Thus, a comprehensive judgment and decision ought to be made based on medical history, physical examination and assisted examination. Surgical exploration is necessary for diagnosis and treatment of RHP. For infertile patients, assisted reproductive technology should be applied when necessary. Caution to prevent the occurrence of pregnancy complications such as uterine rupture, and application of cesarean section to terminate pregnancy are recommended.
Asunto(s)
Aborto Espontáneo , Embarazo Cornual , Embarazo Ectópico , Rotura Uterina , Embarazo , Humanos , Femenino , Adulto Joven , Adulto , Cesárea/efectos adversos , Estudios Retrospectivos , Embarazo Ectópico/diagnóstico por imagen , Embarazo Ectópico/cirugía , Embarazo Cornual/diagnóstico , Embarazo Cornual/cirugía , Útero/diagnóstico por imagen , Útero/cirugía , Rotura Uterina/etiologíaRESUMEN
BACKGROUND: Progressive pseudorheumatoid dysplasia is a rare skeletal dysplasia mainly caused by abnormal autosomal recessive inheritance. Although the main function of cartilage is mechanical support and the characteristics of this disease is the degradation of AC, previous studies on it had been mainly focused on clinical and genetic aspects and the mechanical behavior of the cartilage affected by PPRD is still ambiguous. In this study, we investigate the mechanics and structure of the cartilage suffered disease at multi-scale, from individual chondrocytes to the bulk-scale tissue. METHODS: Depth-sensing indenter were employed to investigate the mechanics of cartilage; we performed atomic force microscope nanoindentation to investigate the cell mechanics and scanning electron microscopy were used to explore the structure feature and chemical composition. FINDINGS: The elastic modulus of chondrocytes harvested from cartilage suffered from progressive pseudorheumatoid dysplasia is significantly higher than from normal cartilage, same trend were also found in tissue level. Moreover, denser collagen meshwork and matrix calcification were also observed. INTERPRETATION: The elastic modulus of cartilage should closely related to its denser structure and the calcification, and may potentially be an indicator for clinical diagnosis. The stiffening of chondrocytes during PPRD progression should play a rather important role in its pathogenesis.
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Cartílago Articular/patología , Progresión de la Enfermedad , Artropatías/congénito , Fenómenos Mecánicos , Fenómenos Biomecánicos , Cartílago Articular/metabolismo , Condrocitos/metabolismo , Condrocitos/patología , Colágeno/metabolismo , Módulo de Elasticidad , Humanos , Artropatías/metabolismo , Artropatías/patologíaRESUMEN
Cadmium, a heavy metal, is a toxic environmental and industrial pollutant. Exposure to cadmium can lead to the toxic effects in a variety of tissues, also including the brain. The present study investigated the effect of cadmium exposure on the histopathology of cerebral cortex in juvenile mice. Juvenile mice were randomly divided into control, low (1.87 mg/kg), medium (3.74 mg/kg), and high (7.48 mg/kg) dose groups. After cadmium exposure by drinking water for 10 days, the cerebral cortex was obtained for histopathology studies. The medium and high dose of cadmium, rather than low dose, could induce the histopathology alterations of cerebral cortex in a dose-dependent manner. In the high-dose group, microstructure significantly showed pia mater encephali divorcing from cerebral cortex layer, serious hyperemia of blood capillary in pia mater encephali and cerebral cortex, broadening vessel peripheral clearance, a large number of eosinophil leukocyte infiltrating around blood vessel, vacuolar degeneration in part granule cells, and obviously increasing apoptotic cells. Ultrastructure obviously displayed marginalized heterochromatin, incomplete or fused nuclear membranes, broadened perinuclear space, ambiguous mitochondria cristae, decreased synaptic cleft, and fused presynaptic and postsynaptic membrane. Our results revealed that cadmium at the middle and high dose could induce obvious microstructure and ultrastructure alterations of cerebral cortex in juvenile mice, which may be one important mechanism of cadmium neurotoxicity.
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Cadmio/toxicidad , Corteza Cerebral/patología , Administración Oral , Animales , Apoptosis , Corteza Cerebral/efectos de los fármacos , Corteza Cerebral/ultraestructura , Relación Dosis-Respuesta a Droga , Eosinófilos/metabolismo , Femenino , Lóbulo Frontal/ultraestructura , Heterocromatina/metabolismo , Hiperemia/inducido químicamente , Leucocitos/metabolismo , Masculino , Ratones , Microscopía Electrónica de Transmisión , Mitocondrias/efectos de los fármacos , Neuronas/metabolismo , Piamadre/efectos de los fármacos , Sinapsis/efectos de los fármacosRESUMEN
We investigated the effects of cadmium on lung cell DNA in immature mice. The mice were randomly divided into four groups: control group, low-dose group (1/100 LD(50)), middle-dose group (1/50 LD(50)), and high-dose group (1/25 LD(50)); they were supplied with cadmium chloride or control water for 40 days. Lung cells collected from sacrificed mice were used to evaluate the extent of DNA damage by comet assay. The ratio of tailing cells, DNA tail length, DNA comet length, DNA tail moment, DNA olive tail moment, and percentage of DNA in the comet tail were measured. The rate of tailing lung cells exposed to cadmium increased significantly; the low-concentration group had significantly (P < 0.05) higher rates, and the middle- and high-concentration groups had higher (P < 0.01) rates compared to the control. DNA tail length, DNA comet length, DNA tail moment, and DNA olive tail moment all increased with the increase in cadmium doses, but compared with those of the control group, no significant differences in low-dose group were found (P > 0.05), and the differences in middle- and high-dose groups were all highly significant (P < 0.01). The degree of DNA damage also increased with the increase of the cadmium concentrations. We conclude that cadmium significantly increases DNA damage in lung cells of immature mice in a dose-dependent manner.
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Cloruro de Cadmio/toxicidad , Daño del ADN , Agua Potable/efectos adversos , Pulmón/patología , Contaminantes Químicos del Agua/toxicidad , Animales , Ensayo Cometa , Femenino , Dosificación Letal Mediana , Pulmón/efectos de los fármacos , Masculino , RatonesRESUMEN
The immunolocalization of human neutrophil elastase (HNE) in the alveolar interstitium of 6 patients with emphysema was investigated by immunochemical electron microscopy. The results showed that HNE is localized in the azurophil granules of neutrophils, and extracellularly on the elastic fibers of alveolar interstitium and basement membranes of epithelium and endothelium. The damage of elastic fibers and basement membranes could be observed. The HNE level of the alveolar interstitium was obviously elevated and closely related to the severity of emphysematous lesions as shown by measuring the mean linear intercept (MLI) in 4 emphysematous lungs with chronic bronchitis (r = 0.84). This suggests that HNE might play an important role in the pathogenesis of emphysema. Although enlarged airspace and increased MLI data were observed in 2 patients, one with asthma and the other, an elderly patient, without lung diseases, the HNE level of alveolar interstitium is much less than that of the other 4 chronic obstructive pulmonary disease patients. This implies that the mechanism of the the airspace enlargement occurring in the 2 patients may be different from that of others. These findings support the hypothesis of elastase-antielastase imbalance on the pathogenesis of pulmonary emphysema.
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Tejido Elástico/enzimología , Pulmón/enzimología , Neutrófilos/enzimología , Elastasa Pancreática/metabolismo , Enfisema Pulmonar/diagnóstico , Adulto , Membrana Basal/enzimología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Enfisema Pulmonar/patologíaRESUMEN
It has been proposed that the development of human emphysema is related to an imbalance between elastase and its inhibitors in the lung. This report describes the immunolocalization of human neutrophil elastase (HNE) in the alveolar interstitium of 6 patients with emphysema by using immunohistochemical, ultrastructure technique. The results showed that HNE is localized in the azurophil granules of neutrophils, and extracellularly on the elastic fibers of alveolar interstitium and basement membranes of epithelium and endothelium in four emphysematous lungs with chronic bronchitis. The damage of elastic fibers and basement membranes can also be observed. The HNE level of the alveolar interstitium is obviously elevated and closely related to the severity of emphysematous lesions by measuring mean linear intercept (MLI), with the correlation coefficient r = 0.84. This suggests HNE can bind to elastic fibers and basement membranes in the emphysematous lung, and damage these tissues, which might play an important role in the development of human emphysema. These findings support the elastase-antielastase imbalance hypothesis concerning the pathogenesis of human emphysema.