Microglandular hyperplasia: a model for the de novo emergence and evolution of endocervical reserve cells

BACKGROUND: Microglandular hyperplasia (MGH) of the cervix in human beings is associated early with gland proliferation and terminates in mature squamous metaplasia. Using antibodies to basal cell markers, we analyzed biopsies with MGH to profile the distribution and evolution of reserve cells and their relationship to these epithelial components. DESIGN: Serial sections of 24 MGHs were subdivided into (1) early MGH with microacinar proliferation, abundant subnuclear vacuoles, and a paucity of supporting stroma and (2) late MGH with more prominent supporting stroma and/or squamous metaplasia. Serial sections were stained with antibodies to p63, bcl-2, and keratin-5. RESULTS: Three patterns of p63 staining were observed corresponding to the age of the MGH: (1) scattered staining of columnar cells, (2) focal subcolumnar staining in a reserve cell distribution, and (3) linear subcolumnar arrays of p63-positive reserve cells that in some MGHs expanded into a squamous metaplasia. Early acinar proliferations showed weak and focal columnar cell staining followed by focal subcolumnar p63-positive cells. In late lesions, p63 staining was compartmentalized to the extraglandular (or subcolumnar) areas. Stainings of p63, bcl-2, and keratin-5 were concordant. Staining for keratin 14, which localizes to squamous cells, was variable. CONCLUSIONS: The immunohistochemical profile in MGH indicates that reserve cells are created in adulthood during specialized columnar proliferations. This columnar to reserve cell transition may produce a stable population of reserve cells or a transition to squamous metaplasia. Similar patterns are seen in cervical neoplasia, suggesting a link between benign and neoplastic cervical epithelial differentiation.     

The related causes in very early morning onset of stroke

We investigated the influence of early awakening and related factors on onset of cerebrovascular disease (CVD). Totally 1199 stroke patients, in whom the onset time was known, at 3 reference hospitals were included in this study. The effects of demographic, medical, and pathophysiological factors on the circadian pattern of an unselected series of patients with ischemic stroke were analyzed. Nine-hundred seventeen CVD patients with cerebral infarction (CI), 240 patients with intracerebral hemorrhage (CH), and 42 patients with subarachnoid hemorrhage (SAH) were identified. The greatest portion of strokes (32.5%) occurred between 03:00 and 06:00 a.m. Nearly one half of the strokes in this series occurred in the very early- to mid-morning hours. This analysis of strokes provides strong evidence with a higher risk in the early morning hours (03:00 a.m. to 06:00 a.m.), and lower risk during the night time period (21:00 p.m. to midnight). Approximately 1 of every 3 strokes (1 of 3 ischemic strokes, 1 of 6 hemorrhagic strokes, and 1 of 8 subarachnoid hemorrhages) is attributable to the early morning excess. This difference tried to be explained by three ways: cold weather, religious factors, and physiological mechanisms.     

Return of the cycad hypothesis – does the amyotrophic lateral sclerosis/parkinsonism dementia complex (ALS/PDC) of Guam have new implications for global health?

Recently published work provides evidence in support of the cycad hypothesis for Lytico--Bodig, the Guamanian amyotrophic lateral sclerosis/parkinsonism dementia complex (ALS/PDC), based on a new understanding of Chamorro food practices, a cyanobacterial origin of beta-methylaminoalanine (BMAA) in cycad tissue, and a possible mechanism of biomagnification of this neurotoxic amino acid in the food chain. BMAA is one of two cycad chemicals with known neurotoxic properties (the other is cycasin, a proven developmental neurotoxin) among the many substances that exist in these highly poisonous plants, the seeds of which are used by Chamorros for food and medicine. The traditional diet includes the fruit bat, a species that feeds on cycad seed components and reportedly bioaccumulates BMAA. Plant and animal proteins provide a previously unrecognized reservoir for the slow release of this toxin. BMAA is reported in the brain tissue of Guam patients and early data suggest that some Northern American patients dying of Alzheimer's disease (AD) have detectable brain levels of BMAA. The possible role of cyanobacterial toxicity in sporadic neurodegenerative disease is therefore worthy of consideration. Recent neuropathology studies of ALS/PDC confirm understanding of this disorder as a 'tangle' disease, based on variable anatomical burden, and showing biochemical characteristics of 'AD-like' combined 3R and 4R tau species. This model mirrors the emerging view that other neurodegenerative disease spectra comprise clusters of related syndromes, owing to common molecular pathology, with variable anatomical distribution in the nervous system giving rise to different clinical phenotypes. Evidence for 'ubiquitin-only' inclusions in ALS/PDC is weak. Similarly, although there is evidence for alpha-synucleinopathy in ALS/PDC, the parkinsonian component of the disease is not caused by Lewy body disease. The spectrum of sporadic AD includes involvement of the substantia nigra and a high prevalence of 'incidental'alpha-synucleinopathy in sporadic AD is reported. Therefore the pathogenesis of Lytico-Bodig appears still to have most pertinence to the ongoing investigation of the pathogenesis of AD and other tauopathies.     

Detection of mutations in whole genome-amplified DNA from laser-microdissected neurons

Laser microdissection allows removal of individual cells for DNA extraction, but obtaining reliably amplified DNA from the small numbers of cells that survive neurodegenerative diseases can be difficult. We therefore tested a recently-available technique to amplify genomic DNA to see if it could reliably detect a mutation in nervous system cells. Fifty cortical motor neurons were removed by laser microdissection from cases of motor neuron disease both with and without known mutations in the gene for superoxide dismutase 1 (SOD1). DNA was extracted and amplified with a linear genomic amplification kit (GenomiPhitrade mark). The PCR product of exon 4 of SOD1 from this DNA was then sequenced. The GenomiPhi kit amplified the extracted DNA approximately 70 times. When exon 4 of SOD1 from this DNA was amplified by PCR the E100G SOD1 mutation could be identified on sequencing. No errors in replication were found. In conclusion, the GenomiPhi method of genomic DNA amplification appears to result in reliable replication of mutations in neurons. This technique can be used to obtain increased amounts of genomic DNA to study mutations within cells of the nervous system.     

Isolated retrovesical cyst hydatid in a child: an unusual presentation of echinococcosis

Echinococcosis is the most widespread, serious human cestode infection in the world. Isolated retrovesical cyst hydatid is extremely rare in children and mostly causes symptoms because of its pressure on adjacent organs. We report on the case of an 8-year-old girl with an isolated retrovesical cyst hydatid. Final diagnosis was established after histological examination, whereas imaging techniques failed to establish the diagnosis.     

Synovial chondromatosis of the hip: a case report and clinicopathologic study

Primary synovial chondromatosis (PSC) is a rare, usually monoarticular disorder of synovial joints. PSC is characterised by the formation of osteocartilaginous nodules in the synovial connective tissue. We report the case of a 32-year-old male with PSC of the left hip. At clinical examination abduction of the left hip was limited and rotation was painful. Ultrasound examination of the hip revealed joint effusion and multiple hyperechogenic foci due to distal acoustic shadowing. Plain radiographs showed a slight soft tissue swelling around the femoral neck and multiple round or ovoid calcifications of a uniform size. MRI revealed a large joint effusion with multiple small filling defects. Open total synovectomy was performed after dislocation of the femoral head. The diagnosis of PSC was confirmed by histological examination of the excised material. The majority of cells failed to exhibit any staining for cerb B-2 and ki-67. None of the sections showed more than 5% labelling for DNA-fragmentation proven by terminal deoxytransferase-mediated dUTD nick-end labeling (TUNEL), and all were completely non-reactive for p53 as well. In conclusion, immunohistochemical analysis suggests that in this case PSC originated from metaplasia and not from a proliferative process. After two years, the patient was free of symptoms and radiological control did not show evidence of recurrence or femoral head necrosis. Physical findings, diagnosis, histological features and management of PSC are discussed.     

One-stage revision of shoulder arthroplasty in the case of periprosthetic infection

AIM: Infection of shoulder arthroplasties is rare, but represents a potentially devastating complication. The aim of this work is to show the value of various diagnostic procedures, specify causative pathogens and present the results of one-stage revised patients. METHOD: We performed a retrospective analysis of our 16 consecutive patients with an infected shoulder arthroplasty. RESULTS: In 13 of 16 cases a causative pathogen could be established preoperatively. Staphylococcus and Propioni spp. dominated. Only 9 patients could be followed up because two died, two were lost and three patients were revised because of non-infectious complications. The follow-up time was 5.8 years (13 months-13.25 years). The Constant-Murley score was 33.6 of 100. Eradication of infection was achieved in all patients. In the follow-up time no reinfection has occurred. CONCLUSION: Culturing of the preoperative joint fluid aspirate and the determination of CRP provide an early diagnosing of shoulder arthroplasty infection. One-stage revision arthroplasty with radical debridement and application of antibiotics to the bone cement provide an accurate therapy of periprosthetic shoulder infection.     

The sternal fracture: radiographic analysis of 200 fractures with special reference to concomitant injuries

BACKGROUND: Previous studies have shown that trauma-hemorrhagic shock (T/HS) causes significant alterations in red blood cell (RBC) deformability and shape. Gender is becoming well recognized as a modulating factor in the pathophysiologic response to trauma. We hypothesize that female subjects are more resistant to adverse effects of T/HS on RBC deformability and shape than male subjects because of estrogen protection. METHODS: Elongation index, a measure of RBC deformability, was examined in six male rats and four groups of female rats at different stages of the estrous cycle (six animals per group) before and 6 hours after T/HS by laser ektacytometry. RBC shape was determined by scanning electron microscopy. Lipid peroxidation was evaluated by measurement of malonyldialdehyde in plasma 6 hours after T/HS. RESULTS: Male rats had a significant decrease in RBC elongation index after T/HS as compared with preshock values. RBC deformability of the proestrous (PES) and estrous female rats did not decrease after T/HS. Postshock RBC deformability values in metestrous and diestrous female rats did not differ from male rats. Male rats and metestrous and diestrous females had a significant increase in the percentage of abnormally shaped RBCs immediately after shock and during the postresuscitation period. In PES and ES female rats, RBC shape distribution did not significantly change after T/HS. Plasma malonyldialdehyde levels at 6 hours post-T/HS were higher in the male rats than in PES female rats. CONCLUSION: These data show that high levels of estrogen in female rats are protective against shock-induced RBC damage and suggest that this effect is associated with a decrease in lipid peroxidation.