Usefulness of Testicular Volume, Apparent Diffusion Coefficient, and Normalized Apparent Diffusion Coefficient in the MRI Evaluation of Infertile Men With Azoospermia.

OBJECTIVE: The purpose of this article is to assess retrospectively the usefulness of testicular volume, apparent diffusion coefficient (ADC), and normalized ADC as measured using MRI in predicting the histopathologic grade of azoospermia and in differentiating obstructive from nonobstructive azoospermia. MATERIALS AND METHODS: A computerized search generated a list of 30 infertile men with azoospermia who had undergone both scrotal MRI and testis biopsy. MRI-determined testicular volumes, ADCs, and normalized ADCs were compared between infertile men with obstructive azoospermia and those with nonobstructive azoospermia. The normalized ADC was calculated as ADC of the testis divided by the ADC of the bladder lumen. RESULTS: Sixteen men had obstructive azoospermia and 14 had nonobstructive azoospermia. The testicular volume was significantly greater in patients with obstructive azoospermia (8.7-27.6 mL) than in patients with nonobstructive azoospermia (1.8-15.4 mL; p < 0.001). The ROC AUC for distinguishing nonobstructive from obstructive azoospermia using testicular volume was 0.92 (a cutoff value of ≤ 13.06 mL yielded sensitivity of 85.71% and specificity of 87.5%). Testicular ADC and normalized ADC were significantly lower in patients with obstructive azoospermia (0.329 × 10-3 to 1.578 × 10-3 mm2/s for ADC; 0.113 to 0.449 for normalized ADC) than in patients with nonobstructive azoospermia (0.801 × 10-3 to 2.211 × 10-3 mm2/s [p = 0.0094] for ADC; 0.235 to 0.61 [p = 0.0001] for normalized ADC). The ROC AUCs for distinguishing nonobstructive from obstructive azoospermia using testicular ADC and normalized ADC were 0.741 (a cutoff value of > 1.031 × 10-3 mm2/s yielded sensitivity of 92.86% and specificity of 56.25%) and 0.875 (a cutoff value of > 0.425 yielded sensitivity of 78.57% and specificity of 93.75%), respectively. CONCLUSION: Testicular volume, ADC, and normalized ADC, as measured using MRI, are useful in predicting the histopathologic grade of azoospermia and in differentiating obstructive from nonobstructive azoospermia.

Superficial Echogenic Lesions Detected on Neonatal Cranial Sonography: Possible Indicators of Severe Birth Injury.

OBJECTIVES: The purpose of this study was to evaluate the characteristics and importance of superficial echogenic lesions around cranial sutures on neonatal cranial sonography. METHODS: We retrospectively reviewed the clinical records and neuroimaging studies of 40 neonates who had superficial echogenic lesions around sutures on neonatal cranial sonography. Magnetic resonance imaging (n = 18) and computed tomography (n = 2) were performed within 2 weeks after sonography. We correlated sonographic findings with computed tomographic and magnetic resonance imaging findings and analyzed them. We also evaluated the associated lesions, neurologic signs, and follow-up changes. RESULTS: Sonographically, the superficial echogenic lesions involved both sulci and perisulcal parenchyma in 39 neonates and were located in the frontal and parietal areas around the sagittal suture in 38 neonates. Magnetic resonance imaging revealed a pattern of hypoxic ischemic encephalopathy in 9 neonates, birth trauma in 3 neonates, a mixed pattern of hypoxic ischemic encephalopathy and trauma in 3 neonates, nonspecific single infarctions in 2 neonates, and lack of a defined lesion in 1 neonate. The associated lesions were subdural hemorrhage (n = 12), epidural hematoma (n = 4), germinal matrix hemorrhage (n = 3), intraventricular hemorrhage (n = 2), and periventricular leukomalacia (n = 1). All epidural hematomas were associated with scalp hematoma, and 2 patients had skull fractures. One neonate with epidural hematoma associated with a hypoxic ischemic encephalopathy pattern showed mild spasticity in both ankles until 16 months. CONCLUSIONS: Superficial echogenic lesions detected around cranial sutures on neonatal sonography may be an indicator of more serious intracranial lesions such as more extensive hypoxic ischemic encephalopathy and intracranial hematomas, including epidural hematoma.

Congenital portosystemic shunts: prenatal manifestations with postnatal confirmation and follow-up.

OBJECTIVES: The purpose of this study was to evaluate prenatal sonographic findings that could be helpful for diagnosis of congenital intrahepatic portosystemic venous shunts and the follow-up results. METHODS: Six neonates with congenital shunts between the portal vein and hepatic vein were enrolled in this study. Prenatal sonography was performed in 5 cases. We categorized the cases according to a previously published classification of intrahepatic portosystemic venous shunts and retrospectively reviewed the prenatal and postnatal sonographic examinations to identify findings that might be helpful for diagnosing shunts prenatally. Follow-up sonographic examinations were done until closure of the shunts. Clinical features were also determined. RESULTS: According to the original reports, intrahepatic portosystemic venous shunts were diagnosed by prenatal sonography in 2 of 5 cases. In the remaining 3 cases, there were suggestive abnormal findings on retrospective review, including an abnormal intrahepatic tubular structure, a prominent hepatic vein, and congestive heart failure. Postnatal sonography showed type 2 shunts in all 6 cases. In 1 case, there were 2 type 2 lesions between two branches of the left portal vein and the middle and left hepatic veins. On follow-up sonography, 5 of the 6 congenital shunts had spontaneously closed by 11 months of age. One case was treated with coil embolization during the neonatal period. Intrauterine growth restriction was the most commonly clinical feature prenatally. CONCLUSIONS: Findings such as an abnormal tubular structure, a prominent hepatic vein, and congestive heart failure can be important clues for identifying congenital intrahepatic portosystemic venous shunts on prenatal sonography. The use of prenatal and postnatal sonography is feasible for detection and evaluation of these shunts.

Uterus didelphys with blind hemivagina and ipsilateral renal agenesis (Herlyn-Werner-Wunderlich syndrome) suspected on the presence of hydrocolpos on prenatal sonography.

We report the case of a female neonate with ipsilateral renal agenesis and uterus didelphys with blind hemivagina, also known as Herlyn-Werner-Wunderlich (HWW) syndrome. Prenatal sonography revealed the absence of the left kidney and a retrovesical cystic lesion suspected as hydrometrocolpos. Postnatal evaluation confirmed that the cystic lesion was a hydrocolpos associated with double uterus and blind hemivagina (HWW syndrome). HWW syndrome can be suspected prenatally if a retrovesical cystic lesion is detected in a female fetus with unilateral absence of kidney.

Incidentally Diagnosed Duodenal Web in Infancy.

A duodenal web is an incomplete diaphragm of the duodenal lumen that causes a partial or (intermittent) complete obstruction. The size of a duodenal web's aperture determines the degree of obstruction, age at presentation, and radiologic findings. We report a case of duodenal web incidentally diagnosed in a 14-month-old boy who presented to the hospital after ingesting a foreign body. We provide a comprehensive report of multiple studies through abdominal radiograph, upper gastrointestinal study, endoscopy, and surgical findings. We emphasize that the duodenum should be considered as the location of the obstruction when infants exhibit delayed discharge or dynamic positioning of a foreign body in a radiologic examination.

Epipericardial Fat Necrosis in a Pediatric Patient Diagnosed Using Contrast-Enhanced MRI Findings: A Case Report and Literature Review.

Epipericardial fat necrosis (EPFN) is a relatively rare cause of acute chest pain, with only five pediatric cases having been reported in the English-language medical literature to date. EPFN can be diagnosed based on the clinical symptoms of acute pleuritic chest pain and classic CT features of typically ovoid fatty lesions surrounded by a rim or capsule in the mediastinal or pericardial areas. Previous studies have reported that contrast-enhanced MRI can detect typical fat signal changes in adults with EPFN. We report a pediatric EPFN case diagnosed using gadolinium-enhanced MRI. Thus, contrast-enhanced MRI may be used to confirm EPFN in the differential diagnoses of the causes of acute chest pain.

Usefulness of Contrast-enhanced Ultrasound in the Evaluation of Chronic Kidney Disease.

BACKGROUND: Contrast-enhanced ultrasound (CEUS) can provide more improved images of renal blood flow and much more information of both macro- and microcirculation of the kidney as compared to Doppler US. OBJECTIVE: To investigate the usefulness of CEUS by analyzing differences in perfusion-related parameters among the three chronic kidney disease (CKD) subgroups and the control group. METHODS: Thirty-eight patients with CKD and 21 controls who were age-matched (20-49 years) were included. Included CKD patients were stratified into three groups according to their eGFR: group I, eGFR ≥ 60 ml/min/1.73 m2 (GFR category I and II); group II, 30 ml/min/1.73 m2 ≤ eGFR < 60 ml/min/1.73 m2 (GFR category III); and group III, eGFR < 30 ml/min/1.73 m2 (GFR category IV and V). Comparisons with the controls (eGFR > 90 ml/min/1.73 m2) were performed. Real-time and dynamic renal cortex imaging was performed using CEUS. Time-intensity curves and several bolus model quantitative perfusion parameters were created using the VueBox® quantification software. We compared the parameters among the CKD subgroups and between the CKD and control groups. RESULTS: Eight patients were included in group I, 12 patients in group II, and 18 patients in group III. Significant differences were noted in the wash-in and wash-out rates between the CKD and control groups (p = 0.027 and p = 0.018, respectively), but not between those of the CKD subgroups. There were no significant differences of other perfusion parameters among the CKD subgroups and between the CKD and control groups. CONCLUSION: A few perfusion related CEUS parameters (WiR and WoR) can be used as markers of renal microvascular perfusion relating renal function. CEUS can effectively and quantitatively exhibit the renal microvascular perfusion in patients with CKD as well as normal control participants.

Urothelial-phase thin-section MDCT of the bladder in patients with hematuria: added value of multiplanar reformatted images.

PURPOSE: To evaluate the diagnostic performance of MDCT with axial images and multiplanar reformatted (MPR) images from the urothelial phase of the bladder in patients with hematuria using cystoscopy as the reference standard. MATERIALS AND METHODS: Our IRB for human investigation approved this study, and informed consent was waived. We included 192 patients (121 men, 71 women; age range 17-90 years; mean age ± SD: 60 ± 14 years) who underwent contrast-enhanced MDCT (scan delay: 70 s; section thickness: 2 mm) and conventional cystoscopy examination for painless gross hematuria or recurrent microscopic hematuria. Two radiologists in consensus interpreted the images for the presence or absence of bladder lesions. Using the kappa statistic, the patient-based agreement was determined between the CT and cystoscopic findings. We compared the diagnostic performance of axial images to those with coronal and sagittal reformations to detect bladder lesions. RESULTS: MDCT showed excellent agreement between cystoscopy-axial scans (κ = 0.896) and axial with reformatted images (κ = 0.948). The sensitivity, specificity, and accuracy of MDCT were 94%, 96%, and 95% in the axial scans and 98%, 97%, and 97% in the axial with reformatted images, respectively. All statistical parameters of diagnostic performance were similar between the axial and the reformatted images (p > .05). CONCLUSION: Axial MDCT imaging demonstrates high diagnostic performance in detecting bladder lesions, but additional reformatted images can improve diagnostic accuracy.

Imaging Features of Carcinosarcoma Arising from Adenofibroma of the Uterus: A Case Report.

BACKGROUND: Adenofibroma is a benign tumor composed histologically of epithelial elements and mesenchymal stroma. Carcinosarcoma is a malignant neoplasm that contains elements of carcinoma and sarcoma. Carcinosarcoma arising from adenofibroma of the uterus has never been reported in the literature in English language. Case Presentaion: We report a case of a 56-year-old woman who complained vaginal spotting persisting for several months. We described here for the first time a case of malignant transformation of uterine endometrial adenofibroma into carcinosarcoma that was depicted as a multilocular cystic lesion with enhancing solid portions and stalk-like structure between the myometrium and endometrial mass.

Ultrasonographic evaluation of acute pelvic pain in pregnant and postpartum period.

Acute pelvic pain in pregnant and postpartum patients presents diagnostic and therapeutic challenges. The interpretation of imaging findings in these patients is influenced by the knowledge of the physiological changes that occur during the pregnant and postpartum period, as well as by the clinical history. Ultrasonography remains the primary imaging investigation of the pregnant and postpartum women. This article describes the causes and imaging features of acute pelvic pain in pregnant and postpartum period and suggests characteristics to such diseases, focusing on the ultrasonography features that allow one to arrive at the corrective diagnosis. Knowledge of the clinical settings and imaging features of acute pelvic pain in pregnant and postpartum period can lead to accurate diagnosis and appropriate management of the condition.

Adenofibroma in the Uterine Cervix Manifesting as Multilocular Cystic Lesions.

Uterine cervical adenofibroma, a very rare benign neoplasm, has rarely been reported in imaging features in the English literature. Herein, we describe a case of uterine cervical adenofibroma that was depicted as a multilocular cystic lesion with enhanced solid portions.

Prenatal diagnosis of aberrant right subclavian artery in an unselected population.

PURPOSE: The purpose of this study was to determine the frequency of aberrant right subclavian artery (ARSA) among unselected fetuses and to evaluate its association with chromosomal abnormalities and other congenital anomalies. METHODS: In all, 7,547 fetuses (gestational age, 20 to 34 weeks) were examined using routine antenatal sonography at our institution between April 2014 and September 2015. The right subclavian artery was assessed using grayscale and color Doppler ultrasonography in the transverse 3-vessel and tracheal view, and confirmed in the coronal plane. RESULTS: ARSA was found in 28 fetuses (0.4%). Further, 27 of these 28 fetuses were euploid (96.4%). Trisomy 18 was the only chromosomal anomaly (3.6%) found in the study sample. ARSA was an isolated finding in 23 of the 28 cases (82.1%). In the remaining three cases (10.7%), ARSA was accompanied with extracardiac anomalies. Other cardiac defects were present in three cases (10.7%). CONCLUSION: Isolated ARSA does not seem to be associated with a significantly increased risk of aneuploidy. However, the possibility of fetal karyotyping, which is a more invasive procedure, should be discussed in the light of the overall risk of the fetus.

Evidence that protease-activated receptor-2 mediates trypsin-induced reversal of stellation in cultured rat astrocytes.

Serine proteases such as thrombin and trypsin play a key role in the development and repair processes in the central nervous system. Molecular actions of serine proteases include multiple cellular events like activation of protease-activated receptors (PARs). PARs belong to a family of G protein-coupled receptors that can be stimulated through their proteolytic cleavage by ligands. PAR-2 has been implicated in neurodegenerative diseases including astrogliosis. Although recent studies have shown that low concentration of trypsin activates PAR-2, its role in morphological changes in primary astrocytes has not been studied. In the present study, we investigated the effects of PAR-2 in astrocyte stellation in rat primary astrocyte culture. Both trypsin (0.1-1 U/ml) and a PAR-2-activating peptide SLIGRL-NH2 (1-50 microM) significantly reversed the stellation induced by serum deprivation in rat astrocytes. Treatment of astrocytes with trypsin or SLIGRL-NH2 resulted in a transient rise of the intracellular Ca2+ level and trypsin-induced morphological changes were blocked by BAPTA, a Ca2+ chelator. In addition, a protein kinase C (PKC) inhibitor, bisindolylmaleimide significantly inhibited the trypsin-induced morphological changes, whereas activation of PKC by phorbol-12-myristate-13-acetate acted as trypsin. Taken together, these results suggest that activation of PAR-2 by trypsin caused reversal of stellation in cultured astrocytes, in part, via the mobilization of intracellular Ca2+ and activation of PKC.

Na+/Ca2+ exchanger 1 alters in pyramidal cells and expresses in astrocytes of the gerbil hippocampal CA1 region after ischemia.

Alterations of immunoreactivity and protein contents of Na(+)/Ca(2+) exchanger 1 (NCX1) were observed in the gerbil hippocampus proper after 5 min of transient forebrain ischemia. NCX1 immunoreactivity was significantly changed in the hippocampal CA1 region, but not in the CA2/3 region after ischemia/reperfusion. In the sham-operated group, NCX1 immunoreactivity was mainly detected in CA1 pyramidal cells. However, 30 min after ischemia/reperfusion, NCX1 immunoreactivity was significantly decreased and then increased at 1 day after ischemia. At this time, NCX1 immunoreactivity in CA1 pyramidal cells was similar to that of the sham-operated group. At 3 days after ischemia, NCX1 immunoreactivity was significantly reduced in the CA1 region compared to that of the sham-operated group and NCX1 immunoreactivity was significantly increased again 4 days after ischemia. Thereafter, NCX1 immunoreactivity was decreased time-dependently in ischemia groups. Between 15 min and 6 h post-ischemia, NCX1 immunoreactivity was expressed in astrocytes in the strata oriens and radiatum of the CA1 region. From 3 days post-ischemia, NCX1 immunoreactivity was expressed in astrocytes in the strata oriens and radiatum. Ischemia-induced changes in NCX1 protein contents in the hippocampus proper concurred with immunohistochemical data post-ischemia. Our results suggest that changes in NCX1 in CA1 pyramidal cells and astrocytes after ischemia are associated with intracellular Na(+) concentrations and that NCX1 may induce an intracellular calcium overload, which may be related to neuronal death.

Ischemia-related changes of glial-derived neurotrophic factor and phosphatidylinositol 3-kinase in the hippocampus: their possible correlation in astrocytes.

In the present study, we observed the changes of endogenous expression of glial-cell-line-derived neurotrophic factor (GDNF) and phosphatidylinositol 3-kinase (PI-3 kinase) in the gerbil hippocampus after transient forebrain ischemia and investigated the correlation between GDNF and PI-3 kinase in the ischemic hippocampus. In the sham-operated group, GDNF and PI-3 kinase immunoreactivity was not found in any cells in the hippocampal CA1 region. GDNF, not PI-3 kinase, immunoreactivity was expressed in non-pyramidal cells in the CA1 region at 6 h after ischemic insult. At 12-24 h after ischemia, GDNF and PI-3 kinase immunoreactivity in the CA1 region was similar to that of the sham-operated group. From 2 days after ischemic insult, GDNF- and PI-3-kinase-immunoreactive astrocytes were detected in the CA1 region, and GDNF and PI-3 kinase immunoreactivity in astrocytes was highest in the CA1 region 4 days after ischemic insult. Moreover, at this time point, GDNF and PI-3 kinase were co-localized in some astrocytes. Western blotting showed that ischemia-related changes of GDNF and PI-3 kinase protein levels were similar to the immunohistochemical changes after ischemia. These results suggest that GDNF and PI-3 kinase may be related to delayed neuronal death and that GDNF and PI-3 kinase may be involved in activation of astrocytes.

Imaging features of complex solid and multicystic ovarian lesions: proposed algorithm for differential diagnosis.

Complex solid and multicystic ovarian lesions are broad-spectrum diseases, ranging from benign to malignant. This article describes the broad-spectrum and imaging features of complex solid and multicystic ovarian lesions and illustrates an algorithmic approach to such lesions, focusing on the ultrasonography and magnetic resonance imaging features that allow one to hone the differential diagnosis. Multimodality imaging workup plays an important role in the characterization and differential diagnosis of these diseases. Also, knowledge of the clinical setting and imaging features for the spectrum of complex solid and multicystic ovarian lesions can lead to appropriate management.

Tyrosine kinase A but not phosphacan/protein tyrosine phosphatase-zeta/beta immunoreactivity and protein level changes in neurons and astrocytes in the gerbil hippocampus proper after transient forebrain ischemia.

In the present study, ischemia-related changes in tyrosine kinase A (trkA) and phosphacan/protein tyrosine phosphatase-zeta/beta (PTP-zeta/beta) immunoreactivities and protein contents were examined in the hippocampus proper after transient forebrain ischemia for 5 min in a gerbil model. Our investigations showed that ischemia-induced changes occurred in trkA immunoreactivity in the hippocampal CA1 region, but not in the CA2/3 region of the hippocampus proper. In the sham-operated group, trkA immunoreactivity was barely detectable. trkA immunoreactivity increased from 30 min after ischemia and peaked at 12 h. Four days after ischemic insult, trkA immunoreactivity was observed in GFAP-immunoreactive astrocytes in the strata oriens and radiatum. In addition, we found that ischemia-related changes in trkA protein content were similar to immunohistochemical changes. On the other hand, PTP-zeta/beta immunoreactivities in the hippocampus proper were unaltered by forebrain ischemia. These results suggest that chronological changes of trkA after transient forebrain ischemia may be associated with an ischemic damage compensatory mechanism in CA1 pyramidal cells.

Expression and changes of Ca2+-ATPase in neurons and astrocytes in the gerbil hippocampus after transient forebrain ischemia.

Ca2+-ATPase is one of the most powerful modulators of intracellular calcium levels. In this study, we focused on chronological changes in the immunoreactivity and protein levels of Ca2+-ATPase in the hippocampus after 5 min of transient forebrain ischemia. Ca2+-ATPase immunoreactivity was significantly altered in the hippocampal CA1 region and in the dentate gyrus, but not in the CA2/3 region after ischemic insult. In the sham-operated group, Ca2+-ATPase immunoreactivity was detected in the hippocampus. Ca2+-ATPase immunoreactivity in the CA1 region and in the dentate gyrus, and its protein levels peaked 3 h after ischemic insult. At this time, CA1 pyramidal cells and dentate polymorphic cells showed strong Ca2+-ATPase immunoreactivity. Thereafter, Ca2+-ATPase immunoreactivity reduced in the CA1 region and in the dentate gyrus. One day after ischemic insult, Ca2+-ATPase immunoreactivity was observed in some CA1 non-pyramidal cells, and 4 days after ischemic insult, Ca2+-ATPase immunoreactivity was detected in astrocytes throughout the CA1 region, but Ca2+-ATPase immunoreactivity in the dentate gyrus had nearly disappeared. Our results suggest that Ca2+-ATPase changes may be associated with a response to ischemic damage in hippocampal CA1 pyramidal cells, and that increased Ca2+-ATPase immunoreactivity in the reactive astrocytes may be associated with the maintenance of intracellular calcium levels.

Role of MAPK/ERK1/2 in the glucose deprivation-induced death in immunostimulated astroglia.

Recently we have reported that glucose deprivation induces the potentiated death and loss of ATP in immunostimulated astroglia via the production of NO and eventually peroxynitrite. This study examined the role of the ERK1/2 signaling pathways in the glucose deprivation-induced death of immunostimulated astroglia. Immunostimulation with LPS+IFN-gamma induced the sustained activation of ERK1/2 for up to 48 h. Glucose deprivation caused the loss of ATP and consequently cell death in immunostimulated astroglia, which was significantly blocked by the treatment with the ERK kinase (MEK1) inhibitor, PD98059 (10-40 microM), to inhibit the ERK1/2 pathways. The systems for generating NO (iNOS) or superoxide (NADPH oxidase) were regulated by the ERK1/2 signaling pathways because the addition of PD98059 reduced the level of both. Interestingly, glucose deprivation caused an approximately two-fold increase in the level of peroxynitrite formation in immunostimulated astroglia, which was significantly reduced by the PD98059 treatment. This demonstrates that the ERK1/2 signaling pathways play an important role in glucose deprivation-induced death in immunostimulated astroglia by regulating the generation of NO, superoxide and their reaction product, peroxynitrite.

Protein disulfide isomerase immunoreactivity and protein level changes in neurons and astrocytes in the gerbil hippocampal CA1 region following transient ischemia.

We investigated the temporal and spatial alterations of protein disulfide isomerase (PDI) immunoreactivity and protein level in the hippocampus proper after 5 min transient forebrain ischemia in gerbils. PDI immunoreactivity was significantly altered in the hippocampal CA1 region. PDI immunoreactivity in the sham-operated animals was found in non-pyramidal cells. At 30 min after ischemia, PDI immunoreactivity was shown in the pyramidal cells of the stratum pyramidale (SP): the PDI immunoreactivity in the pyramidal cells was increased up to 12 h after ischemia. Thereafter PDI immunoreactivity was decreased, and the PDI immunoreactivity was shown in non-pyramidal cells 2 days after ischemia. Four to 5 days after ischemia, almost pyramidal cells in the CA1 region were lost because the delayed neuronal death occurred. At this time period, PDI immunoreactivity was expressed in some astrocytes as well as some neurons. The results of the Western blot analysis were consistent with the immunohistochemical data. These findings suggest that increase of PDI in pyramidal cells may play a critical role in resistance to ischemic damage at early time after ischemic insult, and that expression of this protein in astrocytes at late time after ischemic insult is partly implicated in the acquisition of tolerance against ischemic stress.