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The field of pathology has changed dramatically over the recent decades and has become more complex with emphasis toward subspecialization. These changes potentially influence resident training as programs and trainees search for cutting-edge skills in the evolving field. Over the last 20 years, our institution's residency education was modified profoundly to emphasize subspecialty practice. Furthermore, efforts were made to search for and recruit candidates who desired such training. In this study, we examined a 20-year time period to determine how these changes may have influenced the characteristics of our resident graduates. For each trainee who graduated from our pathology residency program (1994-2013), the following parameters were evaluated: highest academic degree, gender, graduating medical school, type of training, number of publications during residency, enrollment in fellowships, and type of career position. The data collected were divided into 4 time periods. Fisher exact test and 2-tailed t test were used for statistical analyses comparing the first half (1994-2003) to the latter half (2004-2013) of the study. In the second half, there were more graduates who pursued single track pathology training-anatomic pathology or clinical pathology versus combined anatomic/clinical pathology training (P = .035), more first author and total publications per graduate during residency (P < .001), more graduates who enrolled in fellowships (P < .001), and a greater tendency toward an academic career position than all other types combined (P = .034). In parallel to the subspecialization trends in our department, we witnessed changes in the characteristics of our resident graduates whose interests and career choices have become more focused.

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The relative contributions of inflammation and ischemia to the pathogenesis of periventricular leukomalacia (PVL) have not been elucidated. We hypothesized that fetal cardiovascular function and cerebral blood flow velocity (BFV) would be decreased in a rat model of chorioamnionitis. We also tested whether placental inflammation was related to proximity to the cervix in our model of chorioamnionitis [intracervical lipopolysaccharide (LPS) or vehicle (PBS) injection]. On embryonic d 15, Sprague-Dawley rats underwent baseline maternal and fetal echocardiography, followed by LPS or PBS injection, then serial echocardiographic evaluations until embryonic day (ED) 21. One hour after birth, pups had middle cerebral artery (MCA) BFV measured. Placentas of LPS-exposed pups exhibited uniform, higher inflammation grades (p < 0.001). All fetal BFVs increased with advancing GA (p < 0.001) whereas resistance index (RI) decreased (p < 0.001). There was no difference in fetal BFV between the groups other than a reduced gestation-related increase in descending aorta BFV in LPS-exposed rats (p < 0.05). Newborn pups exposed to LPS had lower heart rate (p = 0.006) and MCA BFV (p = 0.024) and higher RI (p = 0.003) and pulsatility index (PI; p = 0.004). In conclusion, intracervical LPS injection produces an inflammation independent of placental position, a blunted increase in gestation-related aortic BFV, and a decrease in MCA BFV in newborn pups.

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OBJECTIVE: Placental fetal vessel thrombosis or vasculitis and retroplacental hematoma have been associated with adverse neonatal outcomes. The activation of thrombin may contribute to the development of thrombosis and inflammation, and can be assessed through the measurement of thrombin-inhibitor complexes. METHODS: A nested case-control study was performed within a cohort of women with singleton gestations. Thrombin-antithrombin III (TAT) and Thrombin-Heparin co-factor II (T-HCII) concentrations were measured in first trimester maternal plasma. Cases were defined by retroplacental hematoma and/or fetal vessel thrombosis or vasculitis in the umbilical cord or chorionic plate. Outcomes were analysed with Mann-Whitney U and linear regression. RESULTS: Concentrations of both TAT (p = 0.013) and T-HCII (p = 0.001) from maternal plasma was significantly lower in cases than in controls. CONCLUSIONS: The development of placental inflammatory and thrombotic lesions at term may be associated with lower concentrations of thrombin-inhibitor complexes earlier in the pregnancy.

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Baseline elevations of C-reactive protein (CRP) during pregnancy have been associated with adverse outcomes, including preterm delivery. Acute elevations have also been associated with intrauterine infections. The relationship between chronic, baseline elevations of CRP and histological chorioamnionitis, however, has not previously been explored. A nested case-control study was performed within a prospective observational cohort of low-risk patients seeking prenatal care. CRP was measured from maternal plasma collected before 13 weeks of estimated gestational age. Cases were defined by histological chorioamnionitis, and controls were selected randomly from patients without chorioamnionitis. We identified 36 cases of chorioamnionitis. There were no significant differences (p=0.64) in CRP concentrations between cases and controls. CRP concentrations remained nonsignificant in a logistic regression model that incorporated prepregnancy body mass index, placental weight, race, and gestational age at delivery (p=0.72). We concluded that the development of histological chorioamnionitis is not associated with elevations in maternal plasma CRP earlier in pregnancy.

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PURPOSE: The purposes of this study were to better understand the fetal development of the anterior cruciate ligament (ACL); to identify the gross anatomy of the ACL; to perform a complete histologic evaluation of the ligament, particularly with respect to the distinction between bundles; and to evaluate ACL length, diameter, cellularity, vascularity, and insertion sites. METHODS: By use of 40 intact knee joints of human fetuses, the gross anatomy of the ACL was inspected under a stereomicroscope (n = 40). The histologic evaluation was performed on the sagittal (n = 20) and transverse (n = 10) sections. RESULTS: The gross observations revealed the presence of 2 distinct bundles: anteromedial (AM) and posterolateral (PL). The femoral origin of each ACL bundle was located in the posterior aspect of the medial surface of the lateral femoral condyle. The footprint of the tibial insertion was ovoid, with the AM bundle located anterior and medial to the PL bundle. The mean length of the ACL was 3.7 mm, the mean width was 1.1 mm, and the mean thickness was 0.9 mm. There was high cellularity, with approximately 5,600 cells/mm2, and intense vascularity. The AM and PL bundles were divided by a well-defined septum. The femoral origin had less dense connective tissue compared with the tibial insertion. CONCLUSIONS: From the time of fetal development, the ACL is composed of 2 bundles, AM and PL. The gross morphology of the ACL in fetuses is similar to that reported in adults; the histology is diverse in cellularity and vascularity. CLINICAL RELEVANCE: This study provides useful information about the anatomy and histology of the fetal ACL.

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