A randomized controlled trial assessing the effectiveness of professional oral care by dental hygienists.

OBJECTIVES: This study was designed to compare professional oral care (POC) by a dental hygienist with tooth brushing and mouth rinsing by patients themselves according to the instructions of a nurse (control). METHODS: Forty patients were randomly assigned to either the POC group (n = 20) or control group (n = 20). The presence of plaque and bacteria was assessed clinically. RESULTS: One patient in the POC group and three patients in the control group dropped out because of exacerbation of underlying disease or death. Plaque control record scores were significantly lower in the POC group than in the control group on the fifth hospital day and the day of discharge. There was no significant difference between the groups in the detection rate of Candida species; and nosocomial pathogens on either day. CONCLUSIONS: Professional oral care by a dental hygienist is more effective than tooth brushing and mouth rinsing by patients themselves according to the instructions of a nurse.

A two-year follow-up of surgical and non-surgical treatments in patients with masticatory muscle tendon-aponeurosis hyperplasia.

This study re-examined the usefulness of surgery for the management of masticatory muscle tendon-aponeurosis hyperplasia (MMTAH) through a comparison of the outcomes between patients who underwent surgery and those who did not. The duration of follow-up was 2 years. Twenty-eight patients who attended the study hospital and were given a diagnosis of MMTAH were included. Nineteen patients underwent surgery (surgical group) and nine patients were instructed to open their mouths wide once a day and did not undergo surgery (non-surgical group). Maximum mouth opening, impairment of daily activities, satisfaction, and the status of mouth opening training were evaluated after surgery. The mean increase in mouth opening after 2 years was 20.2mm in the surgical group and 2.4mm in the non-surgical group. Adequate mouth opening training led to satisfactory results 2 years postoperative, and sustained mouth opening training for 6 months after surgery was a key factor for obtaining good outcomes. The general condition and personality of individual patients should be evaluated carefully before surgery to estimate whether or not they can endure the pain associated with postoperative mouth opening training. The results of this study suggest that the surgical procedure is useful for the management of MMTAH.

Oxidative degradation of non-phenolic lignin during lipid peroxidation by fungal manganese peroxidase.

A non-phenolic lignin model dimer, 1-(4-ethoxy-3-methoxyphenyl)-2-phenoxypropane-1,3-diol, was oxidized by a lipid peroxidation system that consisted of a fungal manganese peroxidase, Mn(II), and unsaturated fatty acid esters. The reaction products included 1-(4-ethoxy-3-methoxyphenyl)-1-oxo-2-phenoxy-3-hydroxypropane and 1-(4-ethoxy-3-methoxyphenyl)-1-oxo-3-hydroxypropane, indicating that substrate oxidation occurred via benzylic hydrogen abstraction. The peroxidation system depolymerized both exhaustively methylated (non-phenolic) and unmethylated (phenolic) synthetic lignins efficiently. It may therefore enable white-rot fungi to accomplish the initial delignification of wood.

Asian hereditary neuropathy patients with peripheral myelin protein-22 gene aneuploidy.

Japanese hereditary neuropathy with liability to pressure palsy (HNPP) patients have a deletion of one peripheral myelin protein-22 (PMP22) gene region in distal chromosome band 17p11.2 as do Caucasian patients. Japanese and Asiatic Indian CMT1A patients have a PMP22 gene duplication that results in Charcot-Marie-Tooth disease type IA (CMT1A; HMSNIA) in patients of European and Middle Eastern ancestry. About 70% of Japanese CMT1 patients have a PMP22 duplication as do Caucasians, while Japanese CMT1B, CMT2 and Dejerine-Sottas patients to not have PMP22 gene region aneuploidy. Although HNPP and CMT1A genotypes are generated simultaneously by unequal recombination that results in PMP22 gene aneuploidy in each daughter cell, only 3 Japanese HNPP probands with PMP22 deletion from a large patient population were referred to a single center compared to 18 referred CMT1A probands with PMP22 duplication. This lower HNPP frequency more likely reflects lower HNPP reproductive fitness than patient ascertainment bias because disease severity and variation in severity is about the same in CMT1A and HNPP patients and because all patients of both types were referred regardless of disease severity. These results, along with an apparently high de novo CMT1A mutation rate, suggest that common ancestors of Japanese, Asian Indians, and Caucasians carried PMP22 geneflanking sequences that enhance unequal crossing over.

Japanese family with an autosomal dominant chromosome instability syndrome: a new neurodegenerative disease?

We report on a Japanese family having an autosomal dominant neurodegenerative disease with chromosomal instability and radiosensitivity. Clinical manifestations of affected members included short stature, osteoporosis, severe dental caries, and various neurological abnormalities, such as mental retardation, depression, dysarthria, hyperreflexia, and ataxic gait. MRI demonstrated a markedly atrophic spinal cord and degeneration of the white matter. Cytogenetic examination showed spontaneous chromosome rearrangements at 14q11.2 and hypersensitivity to radiation and bleomycin. The degree of these cytogenetic abnormalities was significantly higher in the patients than in normal controls but lower than in patients with ataxia telangiectasia or Nijmegen breakage syndrome. Moreover, genetic anticipation was observed in this family: the age of disease onset became earlier, MRI abnormalities more extensive, and the chromosome hypersensitivity to radiation increased in successive generations. We speculate that a basic defect in this family is a mutation in the gene that is responsible for DNA double-strand breakage repair.

Myelinated fibers in Charcot-Marie-Tooth disease type 1B with Arg98His mutation of Po protein.

This study was undertaken to characterize the clinical, electrophysiologic, and histopathologic features of five presumably unrelated Japanese patients with Charcot-Marie-Tooth (CMT) disease type 1B and Arg98His substitution of Po protein and, in particular, to correlate Arg98His substitution to the ultrastructural abnormalities of the myelin sheath. Systematic morphometric studies of the sural nerve, where the CMT type 1B gene abnormality is expressed, have not been performed, especially on the basis of the type of mutation causing CMT type 1B. Electrophysiologic evaluation of limb nerves and morphometric analysis of sural nerves obtained at biopsy were performed. Ultrastructural myelin abnormalities were precisely examined. Clinical symptoms appeared from the second to the fifth decade. All probands presented with gait disturbance. Motor and sensory conduction velocities in the median and ulnar nerves ranged from 10 to 30 m/s. Segmental demyelination and remyelination and marked loss of myelinated fibers were the main findings. On electron microscopy, widening between major dense lines was found between the paired intraperiod lines, where the extramembranous portion of the Po protein resides. This widening is probably directly related to Arg98His substitution. Focal uncompaction of major dense lines coexisted with this widening. This uncompaction, which directly decreases the number of myelin lamellae, may be a secondary effect of Arg98His substitution on the intramembranous domain of Po protein. In conclusion, myelin changes at both extracellular and cytoplasmic appositions of Schwann cell membranes were found in association with Arg98His substitution of Po protein. This study contributes to a better understanding of myelin abnormalities in patients with CMT type 1B and Arg98His or other similar extramembranous amino acid substitutions of Po protein.

[An autopsy case of neuronal type Charcot-Marie-Tooth disease (HMSN type II) with nerve deafness and psychiatric symptoms].

The clinical and pathological findings of a 41-year-old male patient with atypical Charcot-Marie-Tooth disease were reported. There were 3 cases of subarachnoid haemorrhage, 2 nerve deafness and 2 hereditary motor and sensory neuropathy (HMSN) in his family. He had suffered from progressive nerve deafness since 5 years old and gait disturbance since 37 years old. He had been admitted to the psychiatric hospital 3 times because of hallucinatory-delusional state and behavior abnormalities. Neurological examinations at 39 years old revealed that he had mental deterioration (IQ 66), nerve deafness, diffuse muscle atrophy, most marked distally, sensory disturbance, areflexia, positive Romberg's sign, orthostatic hypotension, dysphagia and slurred speech. MCV of median nerve was 27.8 m/sec, and SCV was not evoked. EEG revealed nonspecific dysfunction of the brain. He died of ileus-like condition at 41 years old. General autopsy showed haemorrhagic infarction of the jejunum and ileum due to compression of the superior mesenteric artery and vein by an adhesion band of connective tissue formed after previous appendectomy. Neuropathological examinations revealed axonal degeneration and loss of myelinated fibers with schwannosis of anterior and posterior spinal nerve roots as well as peripheral nerves. The posterior roots were more severely affected than the anterior ones. Ganglion cells of the posterior root ganglia showed remarkable degeneration and loss. There was severe degeneration of the posterior columns, especially in the gracilis, of the spinal cord. Nerve cells in the anterior horns and Clarke's columns also displayed conspicuous atrophy or central chromatolysis followed by gliosis. There was slight degeneration of the posterior spinocerebellar tracts.(ABSTRACT TRUNCATED AT 250 WORDS)

[Randomized prospective trial of gentian violet with dibutyryl cAMP and povidone-iodine with sugar as treatment for pressure sores infected with methicillin-resistant Staphylococcus aureus in elderly patients].

A randomized prospective study was done to evaluate the two treatments for pressure sores infected with methicillin-resistant Staphylococcus aureus in elderly patients: Gentian violet plus dibutyryl cAMP (GVcAMP, n = 8) and povidone-iodine plus sugar (IS, n = 11). Age, underlying diseases, and nutritional status did not differ between the two groups. Specimens were obtained biweekly from the pressure sores and were cultured. The percentage of culture dishes with no methicillin-resistant S. aureus was 93% for the patients given GVcAMP, but only 74% for those given IS (p < 0.01). By the 14th week after the start of treatment, the mean area of the pressure sores in the GVcAMP group had decreased to 45% of the area at the start of treatment. In the IS group, the decrease was smaller to 56% of the area before treatment. No local or systemic adverse effects occurred in either group. GVcAMP is useful to treat pressure sores infected with methicillin-resistant S. aureus.

Preliminary results of a study comparing conventional radiography with phase-contrast radiography for assessing root morphology of mandibular third molars.

OBJECTIVES: The aim of this study was to evaluate the usefulness of phase-contrast radiography for assessing root morphology of mandibular third molars in comparison with conventional radiography. METHODS: We studied 37 extracted mandibular third molars. One oral surgeon compared the number of roots and root curvature of the extracted teeth on conventional radiographs with those on phase-contrast images. RESULTS: The number of roots and root curvature on conventional images differed significantly from those on phase-contrast images. CONCLUSIONS: Our results suggest the possibility that phase-contrast radiography is more useful than conventional radiography for assessing the root morphology of mandibular third molars.

Laccase component of the Ceriporiopsis subvermispora lignin-degrading system.

Laccase activity in the lignin-degrading fungus Ceriporiopsis subvermispora was associated with several proteins in the broth of cultures grown in a defined medium. Activity was not increased significantly by adding 2,5-xylidine or supplemental copper to the medium. Higher activity, associated with two major isoenzymes, developed in cultures grown on a wheat bran medium. These two isoenzymes were purified to homogeneity. L1 and L2 had isoelectric points of 3.4 and 4.8, molecular masses of 71 and 68 kDa, and approximate carbohydrate contents of 15 and 10%, respectively. Data indicated 4 copper atoms per mol. L1 and L2 had overlapping pH optima in the range of 3 to 5, depending on the substrate, and exhibited half-lives of 120 and 50 min at 60 degrees C. They were strongly inhibited by sodium azide and thioglycolic acid but not by hydroxylamine or EDTA. The isoenzymes oxidized 1,2,4,5-tetramethoxybenzene but not other methoxybenzene congeners. A variety of usual laccase substrates, including lignin-related phenols and ABTS [2,2'-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid)], were also oxidized. Kinetic parameters were similar to those of the laccases of Coriolus versicolor. The N-terminal amino acid sequence (20 residues for L1) showed significant homology to those of laccases of other white rot basidiomycetes but not to those of the laccases of Agaricus bisporus or Neurospora crassa.

Subjective side effects of mianserin in relation to plasma concentrations of mianserin and desmethylmianserin.

The main purpose of the present study was to examine the possibility that plasma concentrations of mianserin and its metabolite, desmethylmianserin, might be predicted by recording subjective side effects. In 44 depressed patients, subjective side effects during 3 weeks of treatment with 30 mg of mianserin were evaluated by the UKU Side Effect Rating Scale, and their relationships to plasma concentrations of mianserin and desmethylmianserin were analyzed. There was no significant relationship between plasma concentrations of these compounds and the occurrence of mianserin-induced side effects, except for dryness of mouth during week one. Our study, therefore, suggests that it is difficult to predict plasma concentrations of mianserin and desmethylmianserin based on the occurrence of subjective side effects.

Mutation of the myelin P0 gene in Charcot-Marie-tooth neuropathy type 1.

We had previously reported that the myelin P0 gene was responsible for Charcot-Marie-Tooth neuropathy type 1B (CMT1B). In this study we found a different mutation of the P0 gene in a family of Charcot-Marie-Tooth neuropathy type 1 without a DNA duplication in chromosome 17p11.2. The mutation, a histidine substitution for arginine at amino acid position 98, is located in the extracellular domain of P0 like as the mutations in the three pedigrees with CMT1B. The extracellular domain forms an immunoglobulin domain responsible for the function of P0 as an adhesion molecule. Alterations in the tertiary structure of the extracellular domain of P0 would modify the function of P0, resulting in an impairment of peripheral myelin compaction.

Familial retinoblastoma (mother and son) with 13q14 deletion.

We present here the first familial cases (a mother and son) of dominantly inherited retinoblastoma with a 13q14 deletion [46,XY or XX, del(13)(q14.1q21.2)]. Their esterase D activities in red blood cells were as low as 50% of the normal control and the haplotype of esterase D was a type 1-0 in the mother and a type 2-0 in the son. They had peculiar facies characterized by a high forehead, low and broad nasal root, a short and bulbous nose, a long philtrum, and open mouth with a thin upper lip, and prominent earlobes. Chromosome and esterase D analysis should be performed in patients with retinoblastoma even if retinoblastoma seems to be transmitted through an autosomal dominant inheritance. This family indicates that one of the causes of dominantly inherited retinoblastoma is a chromosome deletion of part of the 13q14 band whether it is detectable by chromosome analysis or not.

Kabuki make-up syndrome: a syndrome of mental retardation, unusual facies, large and protruding ears, and postnatal growth deficiency.

A previously unrecognized mental retardation malformation syndrome was observed in five unrelated Japanese children. Consistent clinical features included moderate-to-severe mental retardation, progressive dwarfism of postnatal onset, a peculiar facies characterized by long palpebral fissures, with eversion of the lateral third of the lower eyelids, arched eyebrows, broad and depressed nasal tip, large prominent earlobes, short fifth fingers, abnormal dermatoglyphics including absence of digital triradius c or d, and frequent otitis media in infancy. Inconsistent abnormalities included epicanthal folds, cleft or high-arched palate, widely spaced teeth, low occipital hair line, scoliosis, and dislocation of the hip joint. Neither familial occurrence nor parental consanguinity was noted. The etiology of the malformation syndrome remains unknown.

Two unrelated cases of single maxillary central incisor with 7q terminal deletion.

Two unrelated cases of single maxillary central incisor (SM-CI) with 7q terminal deletion of the same breakpoint at 7q36.1 were described. They had mental retardation, microcephaly, hypotelorism, short stature, and normal levels of plasma growth hormone. One case had bilateral caudal ectopic kidneys, double renal pelves, and dilated ureters. The other had bilateral hydroureteronephrosis. The present cases suggest that 7q terminal deletion is one of the causes of SMCI.

Long-lasting binding of IT-066 to human histamine H2 receptor.

Based on animal models, IT-066, a histamine H2-receptor antagonist, is reported to possess potent and long-lasting antagonisms on histamine H2 receptor (H2R) -mediated effects. However, no reports have been published concerning its interaction with the human H2R. The aim of this study is to characterize its interaction with human H2R. Chinese hamster ovary cell lines stably expressing human H2Rs were obtained. The effects of IT-066, famotidine, and ranitidine on tiotidine binding and histamine-stimulated cAMP production were analyzed. IT-066 inhibited [3H]tiotidine binding and histamine-stimulated cAMP production more potently than famotidine or ranitidine. In addition, preincubation with 10(-5) M IT-066, but not with 10(-5) M famotidine or 10(-4) M ranitidine, had marked inhibitory effects long after extensive washing. Paraformaldehyde fixation of the cells blunted inhibition of [3H]tiotidine binding induced by preincubation with IT-066, but not that by preincubation with famotidine or ranitidine. IT-066 has potent and long-lasting antagonisms on human H2R. At least one of the IT-066 binding sites is not shared by famotidine, ranitidine, or tiotidine and is affected by paraformaldehyde fixation.