Pathologe最新文献

When Adolf Hitler annexed Austria to the German Reich in 1938, the famous Jewish oral pathologist Bernhard Gottlieb was in great distress. The Viennese university teacher immediately lost his employment and teaching authority and was forced to emigrate.While Gottlieb's exceptional scientific position in oral pathology is well documented, the complex implications of his deprivation of rights and forced emigration in the Third Reich have so far received little attention. Against this background, the present contribution poses the question of the concrete effects of this drastic event on Gottlieb's life and work.In order to clarify this question, Gottlieb's career status, his scientific success up to 1938, the concrete background of his forced emigration, as well as the further course of his life and career in the USA (his immigration country) are scrutinized. In addition, the paper analyzes the extent to which Gottlieb was able to build on his professional career after 1945 and posthumously. The work is based on a thorough analysis of Gottlieb's academic career using archival sources and a re-analysis of the relevant research literature.The study concludes that Gottlieb suffered a severe setback after his emigration. Several reasons played a role. In particular, cultural and age-related adjustment problems, difficult local conditions, and scarce financial resources hampered the seamless continuation of Gottlieb's career in the USA. Only in the last two decades have efforts been made, particularly in the environment of the University of Vienna, to bring Bernhard Gottlieb and his scientific achievements back into collective memory.

Apart from pulmonary disease, acute kidney injury (AKI) is one of the most frequent and most severe organ complications in severe coronavirus disease 2019 (COVID-19). The SARS-CoV‑2 virus has been detected in renal tissue. Patients with chronic kidney disease (CKD) before and on dialysis and specifically renal transplant patients represent a particularly vulnerable population. The increasing number of COVID-19 infected patients with renal involvement led to an evolving interest in the analysis of its pathophysiology, morphology and modes of virus detection in the kidney. Meanwhile, there are ample data from several autopsy and kidney biopsy studies that differ in the quantity of cases as well as in their quality. While the detection of SARS-CoV‑2 RNA in the kidney leads to reproducible results, the use of electron microscopy for visualisation of the virus is difficult and currently critically discussed due to various artefacts. The exact contribution of indirect or direct effects on the kidney in COVID-19 are not yet known and are currently the focus of intensive research.

From the very beginning, special attention regarding severe acute respiratory syndrome-coronavirus‑2 (SARS-CoV-2) and the resulting coronavirus disease-2019 (COVID-19) has been paid to pregnant women.In this review, after a short introduction into the immunodefensive role of the placenta and viral infections in general, we describe the morphological changes of the placenta in SARS-CoV-2-infected pregnant women based on our own and other published studies, draw comparisons to the SARS epidemic, and discuss the question of vertical transmission of SARS-CoV‑2 from the mother to the neonate.The most common pathological findings of the placenta in SARS-CoV‑2 infection are signs of maternal and fetal malperfusion as well as potentially immunologically and/or thromboinflammation-mediated findings. These manifest as infarcts and decidual vasculopathy as well as thrombi in the fetal circulation and avascular villi. In some cases, there is also an inflammatory reaction with villitis, intervillositis, and fetal vasculitis. In addition, it has been shown that SARS-CoV‑2 can directly infect the placenta, so vertical transmission is possible.There is no COVID-19 specific pattern of placental alterations, although the detection of fetal thrombovasculitis, villitis, and intervillositis as well as fetal and maternal malperfusion could be best interpreted as the signature of SARS-CoV‑2 infection - considering the known pathophysiology of COVID-19 regarding other organs (inflammatory reaction and [micro]angiopathy). Detection of viral RNA in the fetal placental tissue and the umbilical cord indicates SARS-CoV‑2 vertical transmission.

During the last decades, the SWI/SNF chromatin-remodeling complex has received enormous recognition as a major player in the molecular pathogenesis of diverse neoplasms. Accordingly, SWI/SNF defects affecting different subunits of the complex became defining genetic features in the nosology of different neoplastic entities. In the kidney, loss of SMARCB1(INI1) as a major component of the SWI/SNF complex has emerged as the defining genetic marker for renal medullary carcinoma and pediatric malignant rhabdoid tumor. Diagnosis of these two rare entities is based on a set of defined demographic, clinicopathological, immunophenotypic, and genetic (SMARCB1 loss) criteria. Moreover, the sickle cell trait is considered a prerequisite for renal medullary carcinoma. Current knowledge illustrates that SMARCB1 loss is encountered in three major tumor categories in the kidney: (1) histologically defined neoplasms that are primarily driven by de novo SMARCB1 loss (renal medullary carcinoma and malignant rhabdoid tumor); (2) SMRACB1-deficient renal cell carcinoma (RCC) with variable non-specific histology ranging from collecting duct-like, papillary high-grade (papillary type 2), or medullary-like (lacking sickle cell trait), to fully undifferentiated; and (3) biphasic (dedifferentiated) RCC showing a variable SMARCB1-deficient undifferentiated component. The latter variant most frequently originates from pre-existing clear cell RCC but may rarely superimpose on papillary or chromophobe RCC. This review summarizes the major defining features of the emerging SMARCB1-deficient renal neoplasms. All SMARCB1-deficient carcinomas have a poor prognosis in common. Therefore, exact diagnosis of these tumors is a prerequisite for studies investigating new therapies.

Paraffin histology is one of the most important and commonly-used laboratory techniques in diagnostic histopathology. The discovery of paraffin embedding is often attributed to the pathologist Edwin Klebs. Klebs was following the lead of Stricker, who embedded embryos in a mixture of hot stearin and white beeswax. We show that Klebs experimented with paraffin wax for embedding tumour tissue. But he quickly rejected it as unsuitable because paraffin wax did not infiltrate the tissue. One of Klebs' correspondents, embryologist Wilhelm His, Sr., learned of Klebs' experiments and decided to try paraffin embedding. His dehydrated chicken embryos in alcohol, cleared them in lavender oil, and dripped hot paraffin wax onto them. This process allowed His to cut good sections. Here, we have replicated His's paraffin embedding protocol in order to determine whether His had indeed made the landmark discovery of infiltration embedding with paraffin wax. We followed the protocol that he gives in his 1868 monograph on the early development of the chicken. The protocol described by His failed, in our hands, to yield sections of the quality that he illustrates in his monograph. Typically, the tissue disintegrated when sectioned due to poor infiltration of the wax. Usable sections could only be obtained if His's protocol was modified by melting the embedded embryos in fresh paraffin wax. One explanation for our findings is that we failed to faithfully replicate His's protocol. Another is that his protocol was incomplete. We suggest that His is likely to have discovered and perfected infiltration embedding with paraffin wax but did not publish a complete protocol.

Throughout his professional life, the pathologist Albert Dietrich devoted himself to researching and combating cancer. Due to his considerable reputation and success, he was one of the first doctors to be awarded the Paracelsus Medal for his scientific services in 1952.However, Dietrich's role in the Third Reich was - and still is - far less defined. In May 1933, he became rector of the Eberhard Karls University in Tübingen, which at that time was one of the most Nazi-oriented universities. However, his term of office was short - by the end of 1933 he had already been replaced by the protestant theologian Karl Fezer.This article sheds light on Dietrich's ambivalent relationship to National Socialism and analyzes and discusses the background to his dismissal, his later (also politically influenced) emeritus status (1938/39), and his entry into the NSDAP, which took place at retirement age (1941). The study is based on archival sources partly evaluated for the first time and on a reanalysis of the relevant research literature.The study shows that Dietrich was targeted by individual Nazi decision-makers primarily because he advocated a supposedly "liberalist" university policy. Dietrich thus ultimately stands for a type of university lecturer who renounced a decidedly Nazi stance in public without, however, placing himself in a critical relationship to Nazi ideology. Against this background, statements from the postwar period that saw him retrospectively near Nazi opposition are to be classified as the formation of legends.