Covid-19 during Pregnancy - Histopathological Lesions of the Placenta.

INTRODUCTION: Pregnant women and their offspring represented a vulnerable patient collective during the Covid-19 pandemic. Beyond the direct effect of SARS-CoV-2 via vertical transmission, an indirect impact on the fetus can occur through placental lesions deteriorating placental villous function. We performed a histopathological analysis of placentas of parturients with SARS-CoV-2 compared to healthy controls. METHODS AND MATERIALS: Between February 2022 and July 2022 we conducted a prospective case-control study analyzing placental specimens of parturients with SARS-CoV-2 infection compared to specimens of placentas of healthy controls. Patient history, Covid-19-specific symptoms, and obstetric outcomes were recorded. Statistical analysis was performed. RESULTS: During the observation period 71 patients were included with a gestational age 37 1/7-41 5/7 weeks. Thirty-six patients presented with SARS-CoV-2 infection. The control group consisted of 35 patients and showed no placental abnormalities. Among SARS-CoV-2-positive parturients, 66.7% of placentas of the case group showed histopathological abnormalities classified as vascular or inflammatory abnormalities. 22.2% of placentas showed acute ischemic infarction areas. 8.3% of placentas showed subchorionic layered thrombi. There was one case of severe acute subchorionitis. SARS-CoV-2 increased the risk of placental lesions significantly (OR 3.000, CI 1.890-4.762, p=0.0001). Placental lesions had no significant impact on perinatal acidosis (OR 0.455, CI 0.044-4.667, p=0.498) or number of cesarean sections (OR 2.314, CI 0.717-7.473, p=0.156). CONCLUSION: SARS-CoV-2 infection during labor and delivery increased the risk of adverse outcomes. Histopathological analysis indicated that the placenta as a maternal-fetal interface was affected by SARS-CoV-2, leading to systemic vasculopathy and inflammation.

Iron deficiency is related to low functional outcome in patients at early rehabilitation after acute stroke.

BACKGROUND: Iron deficiency (ID) is a common co-morbidity in patients with cardiovascular disease and contributes to impaired functional capacity. The relevance of ID in patients in recovery after acute stroke is not known. We assessed the prevalence of ID and anaemia in relation to functional capacity and to recovery during early rehabilitation after stroke. METHODS: This observational study enrolled consecutively 746 patients with ischaemic or haemorrhagic stroke at in-patient early rehabilitation (age 68 ± 13 years, female 47%, ischaemic stroke 87%). Functional capacity was assessed before and after rehabilitation using Barthel index (reha-BI), motricity index (MI), trunk control test (TCT), and functional ambulatory category (FAC). ID was defined as ferritin <100 µg/L or as transferrin saturation (TSAT) < 20% if ferritin was 100- < 300 µg/L or if CrP > 5 mg/L. Anaemia was defined as Hb < 12 g/dL (women) and <13 g/dL (men). RESULTS: The prevalence of ID and anaemia before rehabilitation were 45% and 46%, respectively, and remained high at discharge (after 27 ± 17 days) at 40% and 48%, respectively. Patients with ID had lower functional capacity compared with patients without ID (reha-BI 20 [±86] vs. 40 [±80], MI 64 [±66] vs. 77 [±41], TCT 61 [±76] vs. 100 [±39], FAC 1 [±4] vs. 4 [±4]; median [IQR], all P < 0.001). ID was related to inflammation (OR 2.68 [95% CI 1.98-3.63], P < 0.001), female sex (OR 2.13 [95% CI 1.59-2.85], P < 0.001), haemorrhagic stroke (OR 1.70 [95% CI 1.11-2.61], P = 0.015), initial treatment on stroke unit (OR 3.59 [95% CI 1.08-11.89], P < 0.001), and anaemia (OR 2.94 [95% CI 2.18-3.96], P < 0.001), while age, BMI, and renal function were not related to ID. In adjusted analysis, ID was associated with low functional capacity in all functional scores: reha-BI (OR 1.66 [95% CI 1.08-2.54], P = 0.02), motricity index (OR 1.94 [95% CI 1.36-2.76], P < 0.001), trunk control test (OR 2.34 [95% CI] 1.64-3.32, P < 0.001) and functional ambulatory category (OR 1.77 [95% CI 1.2-2.63], P < 0.02). Functional capacity improved during rehabilitation regardless of presence of ID, but functional outcome remained significantly lower in patients with ID at the end of rehabilitation (rehab BI and MI, both P < 0.001). CONCLUSIONS: Iron deficiency and anaemia are common and persistent findings in patients after acute stroke. ID and anaemia are independently related to lower functional capacity after acute stroke and to poor functional outcome after rehabilitation. Regular assessment of iron status may identify patients at risk of low functional recovery.

Nrf2 Ameliorates DDC-Induced Sclerosing Cholangitis and Biliary Fibrosis and Improves the Regenerative Capacity of the Liver.

The Nrf2 pathway protects against oxidative stress and induces regeneration of various tissues. Here, we investigated whether Nrf2 protects from sclerosing cholangitis and biliary fibrosis and simultaneously induces liver regeneration. Diet containing 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) was fed to Nrf2-KO mice (Nrf2-/-), mice with liver-specific hyperactivated Nrf2 (HKeap1-/-) and wild-type (WT) littermates to induce cholangitis, liver fibrosis, and oval cell expansion. HKeap1-/--mice were protected from almost all DDC-induced injury compared with WT and Nrf2-/-. Liver injury in Nrf2-/- and WT mice was mostly similar, albeit Nrf2-/- suffered more from DDC diet as seen for several parameters. Nrf2 activity was especially important for the expression of the hepatic efflux transporters Abcg2 and Abcc2-4, which are involved in hepatic toxin elimination. Surprisingly, cell proliferation was more enhanced in Nrf2-/-- and HKeap1-/--mice compared with WT. Interestingly, Nrf2-/--mice failed to sufficiently activate oval cell expansion after DDC treatment and showed almost no resident oval cell population under control conditions. The resident oval cell population of untreated HKeap1-/--mice was increased and DDC treatment resulted in a stronger oval cell expansion compared with WT. We provide evidence that Nrf2 activation protects from DDC-induced sclerosing cholangitis and biliary fibrosis. Moreover, our data establish a possible role of Nrf2 in oval cell expansion.

Implications for a Wireless, External Device System to Study Electrocorticography.

Implantable neuronal interfaces to the brain are an important keystone for future medical applications. However, entering this field of research is difficult since such an implant requires components from many different areas of technology. Since the complete avoidance of wires is important due to the risk of infections and other long-term problems, means for wirelessly transmitting data and energy are a necessity which adds to the requirements. In recent literature, many high-tech components for such implants are presented with remarkable properties. However, these components are typically not freely available for such a system. Every group needs to re-develop their own solution. This raises the question if it is possible to create a reusable design for an implant and its external base-station, such that it allows other groups to use it as a starting point. In this article, we try to answer this question by presenting a design based exclusively on commercial off-the-shelf components and studying the properties of the resulting system. Following this idea, we present a fully wireless neuronal implant for simultaneously measuring electrocorticography signals at 128 locations from the surface of the brain. All design files are available as open source.