To delineate the clinicopathological features of diffuse axonal injury in patients with diffuse cerebral injury, we reviewed 19 cases from a series of 726 brain autopsies performed during a recent ten-year period. The criteria for inclusion were loss of consciousness for more than 6 hours in closed head injury patients, and no development of a space-occupying lesion within 7 days of injury. The injury was more prevalent in males(70.6%), and in patients aged between 10 and 50 years(82.4%). The main cause was traffic accident(82.4%), and the patients, Glasgow coma scale score on admission after injury was between 3 and 7. CT or MRI performed within the first 7 days of injury disclosed either one or combined focal lesions in the cerebral white matter, corpus callosum and brain stem in 66.7% of cases, and no identifiable lesion in 33.3%. Axonal swellings are the histologic hallmark of diffuse axonal injury in closed head trauma. In this study, careful brain dissection and neuropathologic studies demonstrated these swellings in all autopsy brains. The immunohistochemical stain for neurofilament proteins(68kD, 160/200kD) is the most sensitive marker of axonal swelling, especially when a patient survives more than 12 hours after injury. However, a neurofilament protein(160/200kD) is also expressed in a few normal pyramidal neurons and axial dendrites. Bielschowsky stain also clearly delineates axonal swellings in patients who have survived more than 2 days after injury. Cerebral edema and the appearance of amyloid body are easily identifiable by Luxol fast blue-PAS stain. In patients who survive for 6 months after injury, axonal swellings are hardly identifiable; about 25% of cases are diagnosed by neuropathologic examination only. The above data indicate that for the diagnosis of diffuse axonal injury, careful gross examination and neuropathologic studies are important.
Amyloid ; Autopsy ; Axons ; Brain ; Brain Edema ; Brain Stem ; Corpus Callosum ; Craniocerebral Trauma* ; Dendrites ; Diagnosis ; Diffuse Axonal Injury* ; Glasgow Coma Scale ; Head Injuries, Closed ; Head* ; Humans ; Magnetic Resonance Imaging ; Neurons ; Unconsciousness

To analyze biochemical changes of liver function following combined radiotherapy and hyperthermia, we reviewed retrospectively 37 patients with hepatocellular carcinoma treated with radiotherapy and hyperthermia between July 1988 and December 1990 at Department of Radiation Oncology, Yonsei University College of Medicine. Mean age was 52.7 years and male to female ratio was 11:1. The patients were classified as follows; to A and B group by Child's classification, to M and L group by irradiated volume, and subclassified into BM, BL, AM and AL group according to the combination of Child's classification and irradiated volume. Radiation dose to the primary tumor was 3060 cGy with daily 180 cGy, 5 fraction per week using 10 MV or 4 MV linear accelerator. Hyperthermia (Thermotron RF-8) was performed more than 4 times in all patients. Biochemical parameters including albHmin (Alb), total bilirubin(T. Bil), aspartate aminotransferase (AST or SGOT), alanine aminotransferase (ALT or SGPT), and alkaline phosphatase (ALP) were regularly followed from 1 week before the treatment to 3 months after the treatment. The results are summerized as follows; 1) In all the patient, mean ALP level peaked at 1 month, decreased at 2 months, slightly increased at 3 months after the treatment. Mean SGOT and SGPT levels peaked at 1 month after the treatment. Mean T. Bil level increased continuously and highest at 3 months after the treatment. Mean Alb level did not show significant changes.; 2) Mean ALP level retired to normal level at 3 month after the treatment in A but increased in B group and the differences were statistically significant(p<0.01). Mean SGOT and SGPT levels peaked 1 month in A and 2 months after the treatment in B group. All the biochemical parameters did not show significant difference between M and L group. Mean ALP level increased at 3 months after the treatment in BM and BL groups and decreased in AM and AL groups. Mean SGOT level increased at 3 months after the treatment in BL groups.; 3) Hepatic failure occurred within 3 months after the treatment in 4 patients, all of whom were in BL group. It is suggested that pre-treatment 1iver function and irradiated volume influence biochemical changes of liver in patients with hepatocellular carcinoma following combined radiotherapy and hyperthermia, and this treatment modality appears generally to be safe but might cause hepatic failure particularly in patient with poor liver function and large treatment volume.
Alanine Transaminase ; Alkaline Phosphatase ; Aspartate Aminotransferases ; Carcinoma, Hepatocellular* ; Classification ; Female ; Fever* ; Humans ; Liver Failure ; Liver* ; Male ; Particle Accelerators ; Radiation Oncology ; Radiotherapy* ; Retrospective Studies

The authors encountered a case of gliosarcoma with hemorrhage arising in the left frontotemporal lobe of a 34-year old woman who five months previously had undergone surgery for an ICH in the same lobe. On CT brain scan, we could a slight hyperdense tumor with irregular enhancement could be detected, and perilesional edema and obvious mass effect were also noted. The tumor was firm and surgically,its margine was somewhat poor. On pathologic and histochemical study, the presence of a gliosarcoma was confirmed.
Adult ; Brain ; Brain Neoplasms ; Edema ; Female ; Gliosarcoma* ; Hemorrhage* ; Humans

Background: Increased sebum secretion is considered the main causative factor in the pathogenesis of acne. There is an unmet pharmacological need for a novel drug that can control sebum production with a favorable adverse effect profile. Objective: To investigate the effect of azidothymidine on lipid synthesis in sebocytes and to identify the underlying mechanism of the inhibitory effect of azidothymidine on insulin-like growth factor (IGF)-1-induced lipid synthesis in sebocytes. Methods: Immortalized human sebocytes were used for the analysis. Thin-layer chromatography (TLC) and Oil Red O staining were performed to evaluate lipid synthesis in the sebocytes. The differentiation, lipid synthesis, mitochondrial biogenesis, and mitophagy in sebocytes were investigated. Results: TLC and Oil Red O staining revealed that azidothymidine reduced IGF-1 induced lipid synthesis in the immortalized human sebocytes. Azidothymidine also reduced IGF-1-induced expression of transcriptional factors and enzymes involved in sebocyte differentiation and lipid synthesis, respectively. Moreover, we found that IGF-1 upregulated the levels of peroxisome proliferator-activated receptor-gamma coactivator-1α, LC-3B, p62, and Parkin, major regulators of mitochondrial biogenesis and mitophagy in immortalized human sebocytes. In contrast, azidothymidine inhibited IGF-1 induced mitochondrial biogenesis and mitophagy in the sebocytes. Conclusion These results suggest that azidothymidine downregulates IGF-1-induced lipogenesis by dysregulating the quality of mitochondria through suppression of mitochondrial biogenesis and mitophagy in immortalized human sebocytes. Our study provides early evidence that azidothymidine may be an effective candidate for a new pharmacological agent for controlling lipogenesis in sebocytes.

Background: Increased sebum secretion is considered the main causative factor in the pathogenesis of acne. There is an unmet pharmacological need for a novel drug that can control sebum production with a favorable adverse effect profile. Objective: To investigate the effect of azidothymidine on lipid synthesis in sebocytes and to identify the underlying mechanism of the inhibitory effect of azidothymidine on insulin-like growth factor (IGF)-1-induced lipid synthesis in sebocytes. Methods: Immortalized human sebocytes were used for the analysis. Thin-layer chromatography (TLC) and Oil Red O staining were performed to evaluate lipid synthesis in the sebocytes. The differentiation, lipid synthesis, mitochondrial biogenesis, and mitophagy in sebocytes were investigated. Results: TLC and Oil Red O staining revealed that azidothymidine reduced IGF-1 induced lipid synthesis in the immortalized human sebocytes. Azidothymidine also reduced IGF-1-induced expression of transcriptional factors and enzymes involved in sebocyte differentiation and lipid synthesis, respectively. Moreover, we found that IGF-1 upregulated the levels of peroxisome proliferator-activated receptor-gamma coactivator-1α, LC-3B, p62, and Parkin, major regulators of mitochondrial biogenesis and mitophagy in immortalized human sebocytes. In contrast, azidothymidine inhibited IGF-1 induced mitochondrial biogenesis and mitophagy in the sebocytes. Conclusion These results suggest that azidothymidine downregulates IGF-1-induced lipogenesis by dysregulating the quality of mitochondria through suppression of mitochondrial biogenesis and mitophagy in immortalized human sebocytes. Our study provides early evidence that azidothymidine may be an effective candidate for a new pharmacological agent for controlling lipogenesis in sebocytes.

Within the past few years, an increasing number of reports of Hodgkin's disease following the diagnosis of, and frequently coexisting with, mycosis fungoides have appeared. Previously, Hodgkin's disease found in the lymph nodes of the patient diagnosed as mycosis fungoides was considered as a transformed form of the mycosis fungoides. But, now it has been proven that Hodgkin's disease and mycosis fungoides are histologically and immunohistochemically distinct disease entities. We report a well-documented case of a man who developed Hodgkin's disease and mycosis fungoides simultaneously as a composite lymphoma. Our case emphasizes the importance of considering the diagnosis of another lymphoma in patients with mycosis fungoides who have lymphadenopathy. The cutaneous mycosis fungoides and the Hodgkin's disease should be treated as an independent disease.
Adult ; Case Report ; Hodgkin Disease/*pathology ; Human ; Male ; Mycosis Fungoides/*pathology ; Neoplasms, Multiple Primary/*pathology ; Skin Neoplasms/*pathology