A comparative study of palatal height in a Saudi and Egyptian population

SUMMARY The present study constitutes an attempt to compare normal traits for palatal height and width at different stages of dentition development of two ethnic groups of the Middle East. The observations were obtained from 346 randomly selected normal subjects, 188 Saudis and 158 Egyptians. The stone models were divided into three categories in both groups — primary, mixed and permanent dentitions. Palatal index values were calculated at two levels. Vernier calipers were used to measure the palatal width. Palatal depth was measured by profile Gauge by Vitrex. The results of this study demonstrate no significant difference between ethnic groups at levels 1 and 2 in relation to the palatal height, width and index. For both groups, palatal index increased significantly from the primary to mixed and permanent dentition at level 1.
At level 2, palatal index and height showed decreases in measurement in the mixed dentition compared with the primary and the permanent dentitions.
Subjective assessment of the palatal height correlated with palatal index. The casts were then labelled so that the shallow group had the smallest palatal index followed by the normal and the deep group had the largest palatal index. The results contribute to the information available on the development of palatal shape within two Middle Eastern populations. Knowledge of the normal range in shape can act as a baseline for studies of certain oral developmental abnormalities.     

Narrowing of the critical region in autosomal recessive spastic paraplegia linked to the SPG5 locus

Background: According to electrophysiological and pathological criteria Charcot Marie Tooth (CMT) disease includes primary demyelinating forms (CMT1) and neuropathies with primary axonal loss (CMT2). In CMT1, genetic analysis provided some associations between characteristic lesions and different proteins. In CMT2, four genes were identified recently (CMT2A, B, D, E); the molecular diagnosis is complex and phenotypical hallmarks are lacking. Objectives: To describe the nerve biopsy in three pedigrees with CMT2E caused by mutations of the neurofilament‐light chain gene (NF‐L): two pedigrees from Campania sharing a Pro22Ser substitution in the head domain of protein and one pedigree from Apulia with a novel Leu268Prol substitution in the central rod domain. In all three pedigrees electrophysiology was consistent with a mixed, demyelinating and axonal neuropathy. Results: The three patients analysed revealed a primary axonopathy characterized by giant axonal swelling filled with densely packed neurofilaments and some atrophic axons. Conclusions: We propose that, in the diagnostic work up of CMT2, giant axons may orientate towards CMT2E. The pathological alterations detected correlate intuitively with an altered function of the neurofilaments which constitute the axonal cytoskeleton and are critical for radial growth and for axonal transport.     

Influence of Propofol on Neuronal Damage and Apoptotic Factors after Incomplete Cerebral Ischemia and Reperfusion in Rats: A Long-term Observation

Background: Propofol reduces neuronal damage from cerebral ischemia when investigated for less than 8 postischemic days. This study investigates the long-term effects of propofol on neuronal damage and apoptosis-related proteins after cerebral ischemia and reperfusion.

Methods: Male Sprague-Dawley rats were randomly assigned as follows: group 1 (n = 32, control): fentanyl and nitrous oxide-oxygen; group 2 (n = 32, propofol): propofol and oxygen-air. Ischemia (45 min) was induced by carotid artery occlusion and hemorrhagic hypotension. Pericranial temperature and arterial blood gases were maintained constant. After 1, 3, 7, and 28 postischemic days, brains were removed, frozen, and sliced. Hippocampal eosinophilic cells were counted. The amount of apoptosis-related proteins Bax, p53, Bcl-2, and Mdm-2 and neurons positive for activated caspase-3 were analyzed.

Results: In propofol-anesthetized rats, no eosinophilic neurons were detected, whereas in control animals, 16-54% of hippocampal neurons were eosinophilic (days 1-28). In control animals, the concentration of Bax was 70-200% higher after cerebral ischemia compared with that in animals receiving propofol over time. Bcl-2 was 50% lower in control animals compared with propofol-anesthetized rats during the first 3 days. In both groups, a maximal 3% of the hippocampal neurons were positive for activated caspase-3.     

Pancreatic necrosis: CT manifestations

Pancreatic necrosis is a potential sequela of acute pancreatitis, which pathologically represents a collection of devitalized tissue. Appropriate therapeutic planning requires definition of this irreversibly damaged gland, the presence of which is not consistently diagnosed on the basis of clinical and laboratory data. Over an 18-month period, 22 patients with pancreatic necrosis were studied by one or more computed tomographic (CT) examinations. Retrospective analysis showed the findings to vary with the developmental stage of the necrotizing process. During the acute phase, there was considerable morphologic overlap of necrosis and pancreatic phlegmon. Typical findings were seen in the subacute and chronic stages and included diffuse enlargement of the gland with largely decreased central density. A thick, smooth surrounding rim produced a characteristic saclike configuration. CT-guided aspiration for culture material was performed in four patients with suspected superinfection. Negative gram stain and culture results in two patients allowed surgery to be performed on a more elective basis.     

Caroli disease: high-frequency US and pathologic findings

Three infants with nonobstructive bile duct dilatation (Caroli disease) are described. The bile duct pathology was associated with autosomal recessive polycystic kidney disease in two patients and with severe destruction of the renal parenchyma of unknown origin in the other. Sonograms of the liver showed, besides bile duct dilatations, intraluminal bulbar protrusions, bridge formation across dilated lumina, and portal radicles partially or completely surrounded by dilated bile ducts. Liver biopsy was performed in two patients, and in one patient, the biopsy sample confirmed the findings noted on sonograms. These findings support the hypothesis that the normal embryogenesis of intrahepatic bile ducts is arrested in the pathogenesis of this disease.