Studies on formaldehyde resins, 19. General base catalysis in hydroxymethylation of melamine with formaldehyde

Hydroxymethylation of melamine with formaldehyde to form N-(hydroxymethyl)melamine (2,4-diamino-6-hydroxymethylamino-1,3,5-triazine) was investigated kinetically by the use of hydrogen phosphate/phosphate buffers in aqueous media at pH 11 ? 12. This reaction was found to follow a general base catalysis which results from the kinetic investigation, showing that the reaction takes place by a concerted mechanism involving base, melamine, and formaldehyde. This mechanism differs from that of the base catalyzed hydroxymethylation of phenol or benzamide with formaldehyde, because the acidic phenol and benzamide easily form their conjugate bases by addition of the basic catalyst in a preceding equilibrium step.     

SYNDROME OF THE SEA-BLUE HISTIOCYTE —The First Case Report in Japan and Review of the Literature—

A case of the syndrome of sea-blue histiocyte is presented in a 53-year-old Japanese woman, which is the first recorded case in Japan. The patient had hepatosplenomegaly, bleeding manifestations, mild thrombocytopenia, fatty metamorphosis and cirrhosis of the liver, as well as abnormal serum lipid profiles. Her parents were consanguineous and her maternal grandmother with hepatomegaly died of hepatic failure. Histologically, peculiar histiocytes containing numerous, intracytoplasmic sea-blue stained granules on May-Giemsa stain were demonstrated in biopsy materials of the bone marrow, lymph node and liver. The sea-blue granules in these histiocytes proved to have histochemical staining characteristics of lipogenic ceroid-like pigment. Ultrastructurally, these granules showed membrane-bound, pleomorphic inclusions of heterogeneous nature, including electron-dense amorphous or variegatedly osmiophilic, frequently laminated materials. Enzyme cyto-chemically, localization of acid phosphatase activity was demonstrated in and around the intracytoplasmic inclusions. With regard to the pathogenesis of the sea-blue histiocytes in this case, it may be suggested that the existence of the abnormality in lipid metabolism plays an imporant role in intralysosomal ceroidogenesis in these histiocytes.     

Diverse functions of the p75 neurotrophin receptor

The pan-neurotrophin receptor p75NTR belongs to a large family of receptors, which includes tumor necrosis factor receptors, Fas and approximately 25 other members. The p75NTR is the first receptor to be cloned molecularly. Recent years have seen the emergence of a consensus regarding the signaling pathways activated by p75NTR and its potential biological function, although receptor characterization had not been targeted for some years. We now know that p75NTR has surprisingly diverse effects, ranging from cell death to regulation of axon elongation. This diversity can be explained by the complex formation of p75NTR with other receptors and multiple signaling molecules that interact with the intracellular domain of p75NTR.     

The induction of intestinal metaplasia in rats by pyloroplasty or pyloroplasty plus vagotomy

The influence of increased gastric pH on induction of intestinal metaplasia in the stomach of male JCL/SD rats was examined following surgical procedures of pyloroplasty or pyloroplasty and vagotomy. Twelve months after pyloroplasty plus vagotomy serum gastric concentrations were significantly higher (group II) than in rats receiving only pyloroplasty (group I) or in sham operated animals (group III). Additionally, trehalase activity was also higher in group II than in groups I and III. The incidence of intestinal metaplasia was significantly higher in groups I and II compared with the sham operated control animals (group III). This study indicates that intestinal metaplasia could be induced by surgical procedures such as pyloroplasty with or without vagotomy. Furthermore, elevation of the pH on gastric mucosa by such procedures may play a significant role in the subsequent development of metaplasia in the stomach.     

Skeletal anomalies in a patient with the Pallister/Teschler-Nicola/Killian syndrome

We report on a 3-8/12-year-old boy with the Pallister/Teschler-Nicola/Killian syndrome and previously unreported bilateral skeletal anomalies consisting of small feet and short but otherwise normal humeri, ulnae, femora, and fibulae. His peripheral blood chromosomes were normal; however, 47,XY,+i(12p) was found in 100% of fibroblasts.     

Augmentation of antibody responses of mice to inhaled protein antigens by simultaneously inhaled bacterial lipopolysaccharides

Serum antibody responses of mice to repeatedly inhaled protein antigens such as bovine serum albumin and ovalbumin, plus or minus bacterial lipopolysaccharide (LPS) in the form of an aerosol were studied. Results showed that the levels of responses to inhaled protein antigens varied, depending on the mouse strain-antigen combination and that LPS inhaled simultaneously with the antigens definitely augmented the responses which were not otherwise very high. LPS extracted from Klebsiella O3 (LPS-K) but not LPS from Escherichia coli O55 (LPS-E), which was inhaled at the time of initial inhalation of antigen, significantly intensified the priming for the secondary antibody response to the antigen subsequently inhaled. Both LPS-K and LPS-E, however, definitely acted to augment the response when they were inhaled repeatedly together with the antigen. Oral administration of antigen or antigen plus LPS-K did not induce any detectable antibody response in our experiment, ruling out the possibility that the antigen and LPS stimulated the immune system via alimentary canal rather than via lung. Tissue distribution of the radioactivity soon after inhalation of 131I-labeled antigen and decay speed of the radioactivity were not significantly changed by LPS-K inhaled simultaneously. This suggested that the augmentation of responses was not mediated by the action of LPS to modulate the air-blood barrier against the entry of antigen via lung. All the results prove for the first time that inhaled LPS displays a definite adjuvant action on antibody responses to inhaled antigens.     

FAMILIAL AMYLOID POLYNEUROPATHY WITH MARKED HYPERTROPHY OF THE PERIPHERAL NERVES

Autopsy findings in a 40-year-old male with heredofamilial amyloidosis and polyneuropathy are reported. He had been suffering from progressive autonomic as well as sensorimotor dysfunctions. Prominent amyloid deposit was found in the kidney, heart, thyroid, and testis, and less in the interstitium and small vessels of almost all organs. The peripheral nerves, some showing prominent hypertrophy, were most severely involved by amyloid deposit in a form of stellate mass, which ultrastructurally consisted of radially arranged amyloid filaments. In the hypertrophied nerves and ganglia, in addition to amyloid, massive accumulation of acid mucopolysaccharide (AMPS) was seen filling up the interstitial space, which was the cause of hypertrophy. Ultrastructurally, AMPS was seen as finely granular substance. An extracted amyloid from the kidney showed 8 nm filament on negative staining and was estimated of having a molecular weight of 14,000.     

Genetic and stimulatory cell type requirements for inducing class I major histocompatibility complex alloantigen-specific in vivo cytotoxic T cell immunity

Current interpretation based on analytical in vitro works that actions of Ia antigens and accessory cells such as macrophages and dendritic cells are crucial for inducing cytotoxic T cell responses to class I major histocompatibility complex (MHC) alloantigens has been challenged by experiments performed in a newly developed system handling in vivo cytotoxic T cell immunity. We first characterized the transplantation immunity for second-set rejection of ascitic tumor allografts as principally induced by allogeneic stimulator cells via direct pathway, and as exclusively mediated by class I MHC alloantigen-specific in vivo cytotoxic T cell activity. By comparison of activities of limiting effective doses (10(4)-10(5) cells per mouse) of various stimulator cells in this defined system, we could demonstrate that genetic disparity at the D region of H-2 to the recipient is just enough for inducing the immunity, and presence of allogeneic or syngeneic Ia antigens in addition to H-2D alloantigens on stimulator cells does not give any premium effect. Further study revealed that allogeneic peritoneal cells rich in macrophages or glass-adherent spleen cells enriched for dendritic cells are not stronger stimulators than allogeneic adherent cell-depleted spleen cells and semi-allogeneic thymocytes. These results fit with the alternative concept that the physiological pathway inducing in vivo cytotoxic T cell immunity for graft rejection entirely depends on class I MHC antigens on live lymphocytes as self-supported stimulators, and does not crucially involve additional stimulator activities of Ia antigens and special accessory cell types, which must be in vivo concerned with induction of other types of transplantation immunity.