Metabolic acidosis in patients receiving anticonvulsants

Blood pH, bicarbonate, PCO₂, serum calcium, alkaline phosphatase and red cell carbonic anhydrase were measured in 37 selected patients receiving anticonvulsants. Patients with metabolic acidosis showed a high incidence of hypocalcemia with increased alkaline phosphatase and a significant reduction of carbonic anhydrase-B activity. High iPTH levels were found in 13 patients, but this was not correlated with acid-base balance status. Anticonvulsant drugs seemed to inactive carbonic anhydrase-B activity. Metabolic acidosis might be one of the factors causing a disturbance of calcium metabolism in these patients.This research was supported by Shimabara Science Promotion Foundation, 1978     

In vitro steroidogenesis by human corpora lutea of pregnancy. Effects of human chorionic gonadotropin and prostaglandin F2alpha.

Human corpora lutea of pregnancy obtained at 5 to 11 weeks of gestation were incubated in vitro in the presence of various concentrations of human chorionic gonadotropin (hCG) and prostaglandin F2alpha (PGF2alpha). Progesterone (P) and 17beta-estradiol (E2) released into the medium during incubation were measured by radioimmunoassay. Pieces of the corpora lutea were also examined ultrastructurally before and after incubation. Release of P and E2 into the medium was significantly increased by the addition of hCG and PGF2alpha in some cases. However, the response to hCG and PGF2alpha appeared to vary according to the age of the corpus luteum. Ultrastructurally, the lutein cells were well maintained with respect to the appearance of the smooth endoplasmic reticulum and mitochondria after 120-min incubations. On the basis of these observations, the following conclusions have been reached: 1) This incubation system seems to be suitable for investigating the direct effects of chemicals on lutein cells in vitro. 2) Both hCG and PFG2alpha directly stimulate steroidogenesis in the human corpus luteum of pregnancy, demonstrating their luteotropic actions in vitro. 3) Observed variations in P and E2 secretion might have been due to the different activities of aromatizing enzymes at different stages of gestation.     

The effects of oral alanine administration on blood glucose,pyruvate, lactate,serum glucagon and insulin in human newborns

Alanine (500 mg/kg body weight) was given orally to 27 healthy full term newborn infants, and the changes in blood glucose, pyruvate, lactate, alanine, glucagon and insulin were determined.Significant increments in blood glucose were found in 15 infants with blood glucose levels below 60 mg/100 ml, 4 of whom showed significant elevation of serum glucagon levels on day 1. This observation suggests that hepatic gluconeogenesis is possible immediately after birth.     

Humoral immune response of patients with dental trauma and consequent replacement resorption

Abstract –  Replacement dental resorption may be a consequence of trauma and may cause dental transplants or reimplants to fail. Previously, we demonstrated the participation of the immunopathological response in inflammatory dental resorption. The induction mechanisms of the two types of dental resorption are well known to be different. The aim of the present study was to observe the immune response of patients who suffered dental trauma with subsequent replacement dental resorption. Four patients with replacement radicular resorption and four healthy individuals with no evidence of radicular resorption participated in the study. The results of ELISA demonstrated that serum from patients with replacement dental resorption contained larger amounts of IgG and smaller amounts of IgM anti-total human-dentin extract and anti-fractions of extract than did serum from control individuals. These results signal the hypothesis that dentin is immunogenic and the serological profile of patients with replacement dental resorption may be identified through biochemical analysis of their blood. Precise screening by this method may allow early diagnosis of dental resorption before it becomes visible radiographically.     

Chronological changes of lacunar infarctions on fluid-attenuated inversion recovery magnetic resonance images]

In 26 patients with lacunar syndromes, emergence of new lacunar infarctions were identified within 13 days from onset by diffusion-weighted magnetic resonance images. The identified lacunar infarctions were repeatedly imaged using fluid-attenuated inversion recovery (FLAIR) sequence up to 600 days from onset. On FLAIR images taken by 23 days from onset, lacunar infarctions showed homogeneous hyperintensity. On the later FLAIR images beyond 25 days from onset they were observed as heterogeneously hyperintense lesions in half of the patients. In the other patients, lacunar infarctions were observed as hypointense areas with a hyperintense rim beyond 41 days from onset, which indicates cystic transformation with surrounding gliosis. These FLAIR images of lacunar infarction differ from those of dilated perivascular space which is observed as an area of simple hypointensity.     

Frequency of common bile duct motion artifacts caused by inferior vena cava pulsation on magnetic resonance cholangiopancreatography.

PURPOSE: We assessed the frequency of common bile duct (CBD) motion artifacts caused by inferior vena cava (IVC) pulsation on magnetic resonance cholangiopancreatography (MRCP). METHODS: We retrospectively evaluated CBD motion artifacts in 4 MRCP sequences from each of 115 consecutive patients. RESULTS: We observed 37 (32.2%) ghost artifacts at the ventral and dorsal aspects of the CBD on transaxial, half-Fourier acquisition single-shot turbo spin-echo (HASTE-ax) images; no such artifacts were observed on transaxial T(2)-weighted turbo spin-echo images. In 10 patients, we observed 9 (7.8%) pseudo-defects of the CBD on 3-dimensional T(2)-weighted turbo spin-echo with navigator-triggered prospective acquisition correction technique MRCP and 6 (5.2%) pseudo-defects on single-shot rapid acquisition with relaxation enhancement MRCP. Pseudo-defects were significantly more frequent in patients with ghost artifacts than without (9 of 37 [24.3%] versus one of 78 [1.3%]; P<0.01, McNemar test). CONCLUSION: Although uncommon, pseudo-defects of the CBD caused by IVC pulsation are observed on MRCP. MRCP interpretation that includes comparison with HASTE-ax images can diminish the potential misinterpretation of such CBD motion artifact as bile duct tumor or biliary stone.     

Monoclonal Antibody OKB19, Reactive with a B-Lymphoid Differentiation Antigen (CD19), Binding to Basal Layer Keratinocytes of Normal Human Skin

Monoclonal antibody (moAB) OKB19 reacts with CD19 antigen, which is the broadest lineage-specific surface marker on B-lymphocytes. In frozen tissue sections, using an immunohistochemical technique, the OKB19-positive cells in the basal layer were sharply demarcated from the negative suprabasal layers. In normal hair follicles, the OKB19 reactivity was also confined to one layer of the dermal side of the outer root sheath. However, this reactivity gradually disappeared in the lower areas. The inner surface of the lumina in the eccrine duct was weakly stained with OKB19. The basal keratinocytes were also stained with OKB19 in the lesional epidermis of the various dermatoses examined in this study, when the basal keratinocytes remained unaffected. Even in the hyperproliferative state of psoriasis, the OKB19 reactivity was confined to the basal layer. Several kinds of tumor cells derived from the skin were not stained with OKB19. No labeling was seen even in the basaloid cells of basal cell carcinoma, which are morphologically similar to basal keratinocytes. B4 and Leu-12, other monoclonal antibodies reacting with CD19, did not recognize any keratinocytes in the normal human skin. MoAB OKB19, therefore, reacts with an antigen present on basal keratinocytes and provides a probe for the isolation of the basal keratinocyte subpopulation. Thus, this antibody should be useful in studies of not only B-lymphocyte differentiation, but also normal and aberrant differentiation of the epidermal keratinocytes.