Concurrent and predictive validity of the Mini Nutritional Assessment Short-Form and the Geriatric Nutritional Risk Index in older stroke rehabilitation patients.

BACKGROUND: Malnutrition may worsen clinical outcomes in stroke patients. Few malnutrition screening tools have been validated in the rehabilitation setting. The present study aimed to assess the concurrent and predictive validity of two malnutrition screening tools. METHODS: We retrospectively collected scores for the Mini Nutritional Assessment Short-Form (MNA-SF) and the Geriatric Nutritional Risk Index (GNRI) in consecutive stroke patients aged ≥65 years in a rehabilitation hospital. Concurrent validity was confirmed against the European Society for Clinical Nutrition and Metabolism diagnostic criteria for malnutrition (ESPEN-DCM). Malnutrition risk within the ESPEN-DCM process was assessed using the Malnutrition Universal Screening Tool. Cut-off values with maximum Youden index, and with sensitivity (Se) >90% and specificity (Sp) >50%, were defined as appropriate for identification and screening of malnutrition, respectively. The Functional Independence Measure and discharge destination were used to explore predictive validity. RESULTS: Overall, 420 patients were analysed. Of these, we included 125 patients in the malnutrition group and 295 in the non-malnutrition group based on the ESPEN-DCM. Cut-off values for the identification and screening of malnutrition were 5 (Se: 0.78; Sp: 0.85) and 7 (Se: 0.96; Sp: 0.57) for the MNA-SF; 92 (Se: 0.74; Sp: 0.84) and 98 (Se: 0.93; Sp: 0.50) for the GNRI, respectively. The GNRI predicted discharge to acute care hospital, whereas the MNA-SF did not predict all outcome measures. CONCLUSIONS: The MNA-SF and the GNRI have a fair concurrent validity in stroke patients, although lower cut-off values than currently used were required for the MNA-SF. The GNRI exhibits good predictive validity for discharge destination.

Hypomutability at the polyadenine tract in SMN intron 3 shows the invariability of the a-SMN protein structure.

Recently, the axonal-SMN (a-SMN) protein, which is generated by the gene responsible for spinal muscular atrophy (SMA), SMN, has been reported. Surprisingly, the a-SMN transcript includes the entire sequence of SMN intron 3. We had expected a high frequency of insertion/deletion mutations at a polyadenine tract in this intron, since simple repetitive sequence motifs are prone to mutations. Such mutations could change the C-terminal structure of the a-SMN protein. However, our study showed that almost all individuals, including healthy individuals, SMA patients and SMA-like patients, carried only alleles with a normal polyadenine tract. Hypomutability of the polyadenine tract in SMN intron 3 suggests the existence of transcriptional mechanisms preventing alterations to the open reading frame of axonal SMN and not allowing variability in the protein structure of a-SMN.

Aspirin enhances the induction of type I allergic symptoms when combined with food and exercise in patients with food-dependent exercise-induced anaphylaxis.

We examined the effect of aspirin as a substitute for exercise in inducing urticaria/anaphylaxis in three patients with food-dependent exercise-induced anaphylaxis (FDEIA). Two of the patients had specific IgE antibodies to wheat and the other had antibodies to shrimp. Administration of aspirin before ingestion of food allergens induced urticaria in one patient and urticaria and hypotension in another, while aspirin alone or food alone elicited no response. The third patient developed urticaria only when he took all three items, i.e. aspirin, food and additional exercise, whereas provocation with any one or or two of these did not induce any symptoms. These findings suggest that aspirin upregulates type I allergic responses to food in patients with FDEIA, and further shows that aspirin synergizes with exercise to provoke symptoms of FDEIA. This is the first report of a synergistic effect of aspirin in inducing urticaria/anaphylaxis, which was confirmed using challenge tests in patients with FDEIA.

Review: melanocyte migration and survival controlled by SCF/c-kit expression.

Melanocytes are derived from neural crest and migrate along the dorsolateral pathway to colonize the final destination in the skin. Stem cell factor and its receptor c-kit were identified as gene products of Sl and W mutant loci; both of them were known to have defects in melanocytes survival. In this review, we focus on the function of stem cell factor and c-kit in melanocyte migration and survival, which has become clearer in the last decade. By analysis of both molecules in wild-type and white spotting mutant mice, ligand and receptor set were shown to play multiple roles in the development of melanocytes in mouse ontogeny. Functional blockade of c-kit by specific monoclonal antibody illustrated distinct c-kit dependent and independent stages in melanocyte development. Finally, SCF transgene expression demonstrated that part of the c-kit dependent step is regulated by spatiotemporally specific ligand expression and also indicated the presence of c-kit independent melanocyte stem cells in postnatal skin.

Radiographic studies of the wrist and elbow in cerebral palsy.

We retrospectively studied and evaluated radiographs of the bilateral wrists and elbows in 96 patients with cerebral palsy. There were 55 patients (57.3%) with athetospastic quadriplegia, 30 (31.3%) with spastic diplegia, and 11 (11.4%) with spastic hemiplegia. Plain antero-posterior and lateral roentgenograms were taken of both wrists and both elbows. Overall negative ulnar variance was seen in 18.2% of wrists, and, the variance was highest in athetospastic quadriplegia. We could not find any case of Kienböck's disease. The radiolunate angle was negative in the wrists of those with athetospastic quadriplegia. Scapholunate dissociation was found in 2 wrists (1%). Four dislocations of the radial head were found in 2 patients (2%). The humero-radial distance and humero-ulnar distance were both narrowed. The formation of osteophytes was mainly found in the humero-ulnar joint, especially in those with athetospastic quadriplegia.

A case of classic Kaposi's sarcoma in a Japanese man: detection of human herpes virus 8 (HHV-8) infection by means of polymerase chain reaction and immunofluorescence assay.

The recently discovered human herpes virus 8 (HHV-8) has been implicated in the pathogenesis of Kaposi's sarcoma (KS). Because classic KS in Japan is rare and the detection of HHV-8 DNA by polymerase chain reaction (PCR) has been successful only in limited cases, the frequency and role of HHV-8 infection in KS in Japan remain unclear. Herein we report a case of classic KS in a Japanese man whose HHV-8 infection was confirmed by the detection of lesional viral DNA and serum antibodies against lytic antigen.

Joint-preserving operation for osteoarthrosis of the hip in adult cerebral palsy.

BACKGROUND: A joint-preserving operation was performed on 15 hips with osteoarthrosis, involving 12 patients who had adult cerebral palsy. METHODS: Eleven hips underwent Chiari pelvic osteotomy only; three hips underwent Chiari pelvic osteotomy with femoral osteotomy and the other one hip underwent femoral varus osteotomy only. The mean follow-up period after surgery was 6 years and 2 months (with follow-up range of 2 years and 3 months to 10 years and 6 months). RESULTS: Good results were achieved in 13 of the 15 hips (86.6%). Two patients with athetotic tetraplegia treated with Chiari pelvic osteotomy had pelvic obliquity. Progressive osteoarthrotic change continued in bilateral hips in one case treated with Chiari pelvic osteotomy. CONCLUSION: We confirm that usual treatment for osteoarthrosis of the hip was also applicable for osteoarthrosis of the hip in cases of adult cerebral palsy, provided sufficient attention is given to the complications accompanying spastic paralysis.

Expression of tyrosinase, TRP-1 and TRP-2 in ultraviolet-irradiated human melanomas and melanocytes: TRP-2 protects melanoma cells from ultraviolet B induced apoptosis.

Tyrosinase related protein (TRP)-1 and TRP-2 are known to regulate the quality of melanin, and recently their potential role in inhibiting apoptosis have also been reported. To study the role of tyrosinase, TRP-1 and TRP-2 in the growth, differentiation and cell death of ultraviolet B (UVB) irradiated melanocytes, the expression of these proteins in amelanotic and melanotic cells was examined. Expression of tyrosinase and TRP-1 correlated with melanin content, which was upregulated after repeated irradiation of melanotic cells by low doses of UVB. In contrast, the expression and activity of TRP-2 correlated with cell proliferation, but not with pigmentation. In one melanotic melanoma cell line, significant suppression of cell proliferation was observed after low or high doses of UVB irradiation, possibly due to apoptotic changes. TRP-2 expression was remarkably reduced in UVB-irradiated cells, and transfection with TRP-2 expression vector rescued these cells from UVB-induced apoptosis. These results indicate that TRP-2 expression is closely associated with the regulation of cell growth/survival of melanocytes exposed to UVB and that TRP-2 plays a role in protecting melanoma cells from UVB-induced apoptosis.

Inhibitor effect of apafant on bronchopulmonary responses to platelet activating factor and to antigen in rats.

Apafant (4-(2-chlorophenyl)-9-methyl-2-(3-morpholino-3-oxopropyl)-6H-thieno[3,2- f] [1,2,4]triazolo[4,3-a][1,4] diazepine, CAS 105219-56-5, WEB 2086), as a specific platelet activating factor (PAF) antagonist, inhibited PAF-induced increases of bronchial inflation pressure (delta Pi), pulmonary artery perfusion pressure (delta Pp) and microvascular permeability (wet-to-dry lung weight ratios), dose-dependently, in rats. Apafant also inhibited antigen-induced increase of delta pi, delta Pp and microvascular permeability in passively sensitized rats. Ozagrel also inhibited PAF- and antigen-induced increase of delta Pi, delta Pp and microvascular permeability. Apafant almost completely inhibited the increase of intratracheal pressure and microvascular permeability, but incompletely inhibited the increase of pulmonary artery pressure. At 1 microgram/ml, the effects of ozagrel were almost comparable to that of apafant at the same concentration, but the inhibitory effect on intratracheal pressure was less than that of apafant. Apafant inhibited PAF-induced increase in perfusate of thromboxane (TX) B2 and leukotrine C4/D4E4 (LTs), and antigen-induced increase of TXB2, LTs, PAF and histamine. Ozagrel also inhibited the PAF-induced increase of TXB2, but not the increase of LTs. Apafant inhibited antigen-induced increase of TXB2 and LTs more strongly than PAF-induced increase. The order of inhibitory effects of apafant against generation and release of chemical mediators was TXB2, LTs, PAF and histamine. These findings suggest that TXA2, LTs and PAF may contribute to the increase of intratracheal pressure and microvascular permeability, and histamine may contribute to the increase of vascular resistance in rats. Apafant may inhibit bronchopulmonary responses through PAF receptor antagonism. In addition, apafant can be considered to be useful for the treatment of some allergic diseases when the drug is employed in clinical use.

Role of histamine H3 receptor on hypoxia-reoxygenation-induced cardiac dysfunction in guinea pigs.

Hypoxia elicited a remarkable decrease in contractility and heart rate in isolated right atria from guinea pigs, a decrease which recovered partially during reoxygenation. Histamine content increased during hypoxia and decreased during reoxygenation. However, hypoxia induced a marked degranulation of mast cells. Pretreatment with alpha-methylhistamine (100-300 nM) recuperated control level contractility and heart rate, and prevented the hypoxia-reoxygenation-induced leakage of creatine phosphokinase (CPK). On the other hand, pretreatment with thioperamide (100-300 nM) decreased contractility and heart rate dose-dependently, and prevented recovery during reoxygenation. These data shows that cardiac histamine may play an important role in the protection against hypoxia-reoxygenation injury through the H3 receptor.

Parallel induction of cecropin and lysozyme in larvae of the silkworm, Bombyx mori.

Lysozyme activity in the hemolymph of Bombyx mori increased in parallel with cecropin activity after injection of the larvae with soluble peptidoglycan or UV-killed bacteria. The lysozyme and cecropin A genes were expressed in parallel in the fat body after injection of peptidoglycan as detected by northern blot hybridization. The elicitor specificity for lysozyme induction was identical to that for cecropin, suggesting a common mechanism for recognition of bacteria and following signal transduction introducing to the simultaneous synthesis of cecropin and lysozyme. Bacterial cells killed by UV-irradiation were also effective as elicitor when added to the fat body culture, suggesting that phagocytosis of bacteria by hemocytes may not be an essential process for the induction of antibacterial protein synthesis in the silkworm.

Site-directed mutagenesis of histidine residues in Clostridium perfringens alpha-toxin.

Mutagenesis of H-68 or -148 in Clostridium perfringens alpha-toxin resulted in complete loss of hemolytic, phospholipase C, sphingomyelinase, and lethal activities of the toxin. These activities of the variant toxin at H-126 or -136 decreased by approximately 100-fold of the activities of the wild-type toxin. Mutation at H-46, -207, -212, or -241 showed no effect on the biological activities, indicating that these residues are not essential for these activities. The variant toxin at H-11 was not detected in culture supernatant and in cells of the transformant carrying the variant toxin gene. Wild-type toxin and the variant toxin at H-148 bound to erythrocytes in the presence of Ca2+; however, the variant toxins at H-68, -126, and -136 did not. Co2+ and Mn2+ ions stimulated binding of the variant toxin at H-68, -126, and -136 to membranes in the presence of Ca2+ and caused an increase in hemolytic activity. Wild-type toxin and the variant toxins at H-68, -126, and -136 contained two zinc atoms in the molecule. Wild-type toxin inactivated by EDTA contained two zinc atoms. These results suggest that wild-type toxin contains two tightly bound zinc atoms which are not coordinated to H-68, -126, and -136. The variant toxin at H-148 possessed only one zinc atom. Wild-type toxin and the variant toxin at H-148 showed [65Zn]2+ binding, but the variant toxins at H-68, -126, and -136 did not. Furthermore, [65Zn]2+ binding to wild-type toxin was competitively inhibited by unlabeled Zn2+, Co2+, and Mn2+. These results suggest that H-68, -126, and -136 residues bind an exchangeable and labile metal which is important for binding to membranes and that H-148 tightly binds one zinc atom which is essential for the active site of alpha-toxin.

Roles of the carboxy-terminal region of Clostridium perfringens alpha toxin.

Treatment of Clostridium perfringens alpha toxin with aminopeptidase resulted in no effect on various activities of the toxin. Aminopeptidase did not hydrolyze the native toxin or the toxin treated with urea in the presence of EDTA. Treatment with carboxypeptidase for 30 min resulted in a 75% decrease in these activities. Incubation of the native toxin with carboxypeptidase for 30 min released approximately 15 amino acids from the C-terminus of the toxin. The biological activities of a mutant toxin lacking 20 C-terminal residues of the toxin (AT1-350) showed about 59-87% of the activity of native toxin. The mutant toxin showed partial antigenic identity with the native toxin. These data suggest that the C-terminal domain contributes to maintaining the active form of the toxin.

Spectroscopic characterization of heterochiral DNAs.

We have synthesized heterochiral dodecadeoxynucleotides having an unnatural L-nucleotide residue, and have investigated their structures by ultraviolet (UV) absorption, circular dichroism (CD) measurements and nuclear magnetic resonance (NMR) spectroscopy. It was clearly shown that the overall structures of the heterochiral 12-mers are a right-handed B-conformation and the unnatural L-nucleotide residue in the heterochiral 12-mer (L-4) forms stable Watson-Crick type base-pairing with the natural complementary residue. In this double helix (L-4), the unnatural G4 residue has an S-type sugar conformer and a low-anti glycosidic torsion angle. From the properties of an enantiomer, natural nucleotides may possibly form a low-anti left-handed B-form duplex with the aid of certain factors.

[Experience of the malignant complete intrathoracic goiter: discussion on 13 cases of Japan].

A 56-year-old woman was found to have a mediastinal mass on routine examination. Chest X-ray, CT scan, MRI and superior vena cavography showed a right upper mediastinal tumor invading the SVC. And it was diagnosed malignant intrathoracic goiter by histological examination by percutaneous needle biopsy. On thoracotomy and mediastinotomy, the tumor located only in the right upper mediastinum and had no relation to the cervical thyroid gland. Histological examination revealed papillary adenocarcinoma. We reported a malignant complete intrathoracic goiter and added discussion on another 12 cases seen in Japanese literature.

Glycogen-rich clear cell carcinoma arising from minor salivary glands of the uvula. A case report.

Glycogen-rich clear cell carcinoma arising from minor salivary glands of the uvula in a 35-year-old woman is reported. This tumor was composed of nests and cords of clear cells containing cytoplasmic glycogen but no mucin. The epithelial nature of this lesion was obvious because of positive immunoreactivity for cytokeratin and epithelial membrane antigen, and the presence of immature lumina and intercellular spaces lined by many microvilli, associated with desmosomal junctions and basal lamina, as revealed by ultrastructural study. However, no myoepithelial cells could be detected. From these findings, it may be concluded that this tumor corresponds to glycogen-rich clear cell carcinoma (a variant of clear cell tumor), revealing glandular differentiation.