From the Corners of the Russian Novel: Minor Characters in Gogol, Goncharov, Tolstoy, and Dostoevsky

This dissertation examines a famous formal peculiarity of nineteenth-century Russian novels: the scores upon scores of characters they embrace. Drawing on terminology developed by Alex Woloch--"character space" and "character system"--I ask how Russian writers use their huge, unwieldy systems of characters to create meaning. In each of the four central chapters I analyze a different "overcrowded" nineteenth-century Russian novel: Gogol's Dead Souls, Part I (1842), Goncharov's Oblomov (1859), Tolstoy's Anna Karenina (1875-77), and Dostoevsky's The Brothers Karamazov (1879-80). I address questions such as: what artistic purpose do the many superfluous-seeming minor characters in Gogol's, Goncharov's, Tolstoy's, and Dostoevsky's works serve? What effect does their presence have on the structure of the novels themselves? Why was Dostoevsky so worried by the criticism, which he received throughout the 1870s, that he was "overpopulating" his novels? And how did Dostoevsky's own compositional dilemmas inform both the architectonics and the thematics of The Brothers Karamazov? As I argue, there is an increasingly strong sense in nineteenth-century Russian letters that literary characters not only resemble human beings, but even demand of us the same sort of moral obligations that people do. The perceived personhood of literary characters gives particular significance to the narrative decisions realist Russian writers make (such as how to characterize the major vs. minor figures in a novel, and how much or what kind of narrative attention to grant to each), and Gogol, Goncharov, Tolstoy, and Dostoevsky take full artistic advantage of it. They use the enormous number of characters who appear on the pages of their novels in order to pose, through the narrative structure of their works, many of the most important moral, social, and political questions that preoccupy them: What, in essence, is a human being? Are we capable of recognizing (or even simply acknowledging) the psychological complexity of the many, many people who surround us? Can we establish universal brotherhood on earth, a harmonious, unified society that truly includes everyone, even the most disruptive and destructive ones

Neurodegenerative disease after hematopoietic stem cell transplantation in metachromatic leukodystrophy

Objective: Metachromatic leukodystrophy is a lysosomal storage disease caused by deficient arylsulfatase A. It is characterized by progressive demyelination and thus mainly affects the white matter. Hematopoietic stem cell transplantation may stabilize and improve white matter damage, yet some patients deteriorate despite successfully treated leukodystrophy. We hypothesized that post-treatment decline in metachromatic leukodystrophy might be caused by gray matter pathology. Methods: Three metachromatic leukodystrophy patients treated with hematopoietic stem cell transplantation with a progressive clinical course despite stable white matter pathology were clinically and radiologically analyzed. Longitudinal volumetric MRI was used to quantify atrophy. We also examined histopathology in three other patients deceased after treatment and compared them with six untreated patients. Results: The three clinically progressive patients developed cognitive and motor deterioration after transplantation, despite stable mild white matter abnormalities on MRI. Volumetric MRI identified cerebral and thalamus atrophy in these patients, and cerebellar atrophy in two. Histopathology showed that in brain tissue of transplanted patients, arylsulfatase A expressing macrophages were clearly present in the white matter, but absent in the cortex. Arylsulfatase A expression within patient thalamic neurons was lower than in controls, the same was found in transplanted patients. Interpretation: Neurological deterioration may occur after hematopoietic stem cell transplantation in metachromatic leukodystrophy despite successfully treated leukodystrophy. MRI shows gray matter atrophy, and histological data demonstrate absence of donor cells in gray matter structures. These findings point to a clinically relevant gray matter component of metachromatic leukodystrophy, which does not seem sufficiently affected by transplantation

Neurodegenerative disease after hematopoietic stem cell transplantation in metachromatic leukodystrophy

Objective: Metachromatic leukodystrophy is a lysosomal storage disease caused by deficient arylsulfatase A. It is characterized by progressive demyelination and thus mainly affects the white matter. Hematopoietic stem cell transplantation may stabilize and improve white matter damage, yet some patients deteriorate despite successfully treated leukodystrophy. We hypothesized that post-treatment decline in metachromatic leukodystrophy might be caused by gray matter pathology. Methods: Three metachromatic leukodystrophy patients treated with hematopoietic stem cell transplantation with a progressive clinical course despite stable white matter pathology were clinically and radiologically analyzed. Longitudinal volumetric MRI was used to quantify atrophy. We also examined histopathology in three other patients deceased after treatment and compared them with six untreated patients. Results: The three clinically progressive patients developed cognitive and motor deterioration after transplantation, despite stable mild white matter abnormalities on MRI. Volumetric MRI identified cerebral and thalamus atrophy in these patients, and cerebellar atrophy in two. Histopathology showed that in brain tissue of transplanted patients, arylsulfatase A expressing macrophages were clearly present in the white matter, but absent in the cortex. Arylsulfatase A expression within patient thalamic neurons was lower than in controls, the same was found in transplanted patients. Interpretation: Neurological deterioration may occur after hematopoietic stem cell transplantation in metachromatic leukodystrophy despite successfully treated leukodystrophy. MRI shows gray matter atrophy, and histological data demonstrate absence of donor cells in gray matter structures. These findings point to a clinically relevant gray matter component of metachromatic leukodystrophy, which does not seem sufficiently affected by transplantation