Dialysate and substitution fluid quality for on-line haemodiafiltration and haemofiltration

Summary: A multicentre study concerning the fluid quality for on-line haemodiafiltration/haemofiltration (GDF/HF) treatment was carried out to assure safety and biocompatibility, and a standard for fluid quality has been established. Endotoxin (ET) concentration in the substitution fluid of not less than 1 IU/L caused minimally, yet significantly greater body temperature rises than those less than 1 IU/L (0.52 ± 0.49 vs 0.08 ± 0.40°C, P > 0.01) when 20L of volume was replaced by 4h post dilution HDF treatment. the post treatment plasma levels for tumour necrosis factor-α but not interleukin-6 were correlaed with the amplitude of temporal body temperature rise ( r = 0.75, P > 0.01). By sticking to the standard for on-line HDF/HF treatment that calls for the ET levels in the proportioned dialysate before and the substitution fluid after serial ultrafiltration to be > 50 IU/L and 1 IU/L, respectively, no such deleterious symptoms as fever and hypotension have been observed. Moreover, no enhancement of the plasma ET levels was detected after the first and 6 months of on-line HDF treatment. In conclusion, the newly established advisory standard assures safety and improved biocompatibility of the on-line HDF/HF treatment.     

Long-term prognosis of oral squamous cell carcinoma histologically judged to have been eliminated by the treatment with bleomycin alone

This study was intended to reveal the long-term prognosis in 21 patients with oral squamous cell carcinoma evaluated histologically as having disappeared by bleomycin treatment. Of 16 cases treated with bleomycin alone, recurrence was observed in 4, and cervical metastases in 2, with survival achieved for 5 years or more in 7 (more than 10 years in 3). No recurrence was observed in 5 patients in whom surgery was additionally performed after the bleomycin treatment, but cervical metastasis was found in one of them. In the cases with epithelial dysplasia after bleomycin therapy, recurrence and metastasis were frequent compared to those with normal epithelium, and this discrepancy was of statistical significance. It has been proved that there are long-term survivors among patients with oral carcinoma treated with bleomycin alone.     

Airway hyperresponsiveness to acetylcholine induced by aerosolized arachidonic acid metabolites in guinea-pigs

Background and objective To investigate the role of arachidonic acid (AA) metabolites in airway hypersensitivity. Method We studied the change in airway responsiveness to acetylcholine (ACh) after inhalation of some AA metabolites in guinea-pigs. Results Exposure to prostaglandin (PG) D₂, thromboxane (TX) A₂ mimetic U-46619, leukotriene (LT) D₄ or LTE₄ at concentrations which did not influence bronchial tone and blood pressure dose-dependently caused airway hyperresponsiveness. However, the change was not observed after challenge with a high concentration of PGF_2α Furthermore, PGD₂ and U-46619 induced an acute and short-lived increase in responsiveness, while LTD₄ and LTE₄ induced a slow-onset and longer-lived increase. In the tachyphyiaxis study, although the tachyphylaxis for airway hyperresponsiveness provoked by PGD₂ and U-46619 was not observed, airway hyperresponsiveness induced by the second LTD₄ tended to decrease, and the second LTE₄-induced airway hyperresponsiveness obviously diminished. In the study using antagonists and inhibitors, TX-receptor antagonist BM-13177 inhibited PGD₂- and U-46619-, but not LTD₄- and LTE₄-induced airway hyperresponsiveness. TX synthase inhibitor OKY-046 had no effect on PGD₂-, U-46619- and LTD₄-induced airway hyperresponsiveness, while LTE₄-induced airway hyperresponsiveness tended to be inhibited by these inhibitors. However, the LT-receptor antagonist ONO-1078 inhibited both LTD₄- and LTE₄-, but not PGD₂- or U-46619-induced airway hyperresponsiveness. 5-lipoxygenase inhibitor AA-861 tended to prevent LTE₄-induced airway hyperresponsiveness, but had no effect on PGD₂-, U-46619- and LTD₄-induced enhanced responses. Conclusion These findings indicate that the local existence of PGD₂, TXA₂, LTD₄ and LTE₄ in the guinea-pig airway may act as an airway hyperresponsiveness- inducing factor rather than as a bronchoconstrictor. In addition, PGD₂/U-46619 may stimulate the TX receptor to induce an acute and short-lived airway hyperresponsiveness, and LTD₄ and LTE₄, which may involve secondary mediator release, may act at the LT receptor to induce a slow-onset and longer-lived airway hyperresponsiveness, which may be associated with the induction, the development and the long duration of airway hyperreactivity.     

Prefrontal Cortex and Emotional Behaviors

With 13 tame cats as the subjects, of which 10 had bilateral prefrontal lesions, and 3 as the control group with temporal lesion only, a study was carried out on changes occurring in spontaneous behaviors and hypothalamic rage threshold (HRT) after receiving lesions. As a result it has been demonstrated that behavioral changes appear as hyperreactivity, emotional hyperreactivity and perseverative tendencies. As for the changes in the HRT there can be observed instability of HRT, an increase in reactivity, and a rise in HRT of the group without behavioral change. On the basis of these results it has been pointed out that the lateral surface of prefrontal cortext is involved in the process of the organism in incorporating changes of external circumstance into the HRT, and the orbital surface acts inhibitorily on the HRT.     

Pharmacological responsiveness of the myoepithelium of the isolated human axillary apocrine sweat gland

Human axillary apocrine glands are endowed with well developed myoepithelium, but its pharmacological responsiveness has remained unknown. The present study is part of our efforts in determining the role(s) played by exocrine myoepithelium in the overall secretory processes. Single human apocrine glands were isolated from biopsy skin specimens and were stimulated with various pharmacological agents in vitro. Tubular contraction was recorded photomicrographically and was interpreted as being due to myoepithelial contraction. The tubular contraction was induced by stimulation with phenylephrine (5 × 10^?6M) or adrenaline (5 × 10^?6M) but not with isoproterenol (5 × 10^?6M) or acetylcholine (5 × 10^?6M). A higher concentration of acetylcholine (10^?4M) produced a minor degree of contraction. The phenylephrine-induced contraction was blocked by phentolamine (10^?5M) or by EGTA (5 mM) but not by propranolol (10^?5M) or by atropine (10^?5M). It was concluded that the contractile response of the apocrine myoepithelium is selectively controlled by the alpha-adrenergic stimulation. The possibility is discussed that the major function of the apocrine myoepithelium is not just the pumping out of the preformed sweat but is, as in the eccrine sweat gland myoepithelium, the provision of structural support for the apocrine secretory epithelium to withstand the increase, if any, in the luminal hydrostatic pressure during apocrine sweat secretion.     

Serum prolactin levels in eighty patients with sarcoidosis

Serum prolactin levels were measured by radioimmunoassay in eighty patients (thirty-four males, forty-six females) with sarcoidosis before treatment. In twelve patients (15%) serum prolactin levels were more than two standard deviations above the mean of normal subjects. Hyperprolactinaemia was found most frequently (22%) in patients with radiological stage II; however, 14% of patients with stage I also had elevated serum prolactin levels. In most cases serum prolactin levels fell to within the normal range after treatment with corticosteroid in parallel with improvement of intrathoracic lesions. These findings suggest that hyperprolactinaemia may be due to hypothalamic involvement by sarcoid granulomata. We conclude that the measurement of basal serum prolactin levels using radioimmunoassay is a sensitive and practical method for screening patients with sarcoidosis for hypothalmic lesions.     

Mucoepidermoid Carcinoma of the Esophagus

The esophageal tumor which occurred in a 53-year old female and was histologically similar to the salivary mucoepidermoid carcinoma, showed local invasion at autopsy. No distant metastasis was noted. Our literature review showed invasive and metastatic nature of the tumor. Submucosal location of the tumor in our case supported the proposed origin of the neoplasm from the esophageal gland.     

Toxic Effects on the Visual System of Diaminodiphenoxybutane, Quinine, and Ethambutol in Conscious Dogs

Toxic Effects on the Visual System of Diaminodiphenoxybutane,Quinine, and Ethambutol in Conscious DOGS. SATO, S. (1985).Fundam Appl. Toxicol. 5, 777–784. The effects of diaminodiphenoxybutane(DAPB), quinine, and ethambutol (EB) on the electroretinogram(ERG) and the visual evoked potential (VEP) were examined inconscious dogs. In dogs receiving repeated oral doses of 100mg/kg/day for 4 days or a single iv dose of 30 mg/kg of DAPB,the amplitudes of the ERG a- and b-waves were markedly depressedand the peak latency of the VEP first wave was prolonged. Thereafter,ophthalmoscopic changes consisted of mottled discoloration ofthe fundus, loss of visual placing reaction, and dilatationof the pupils with reduction of the pupillary light reflex wereobserved. These abnormal signs disappeared even though the markeddepression in amplitudes of the ERG a- and b-waves and the prolongationin latency of the VEP first wave continued. A single iv doseof quinine at 50 mg/kg caused a slight depression of the amplitudeof the ERG, whereas the VEP remained relatively unaffected.In a dog receiving a single iv dose of quinine at 100 mg/kg,both the ERG and VEP were depressed, and a slight dilatationof the pupils with reduction of the pupillary light reflex andan impairment of visual placing reaction were observed transiently.There was no abnormality in the ocular fundus in either animalreceiving quinine. The dogs receiving repeated sc doses of EBat 100, 200, and 400 mg/kg/day for 4 weeks each, for a totalof 12 weeks, showed extensive decoloration of the tapetal fundus.However, neither the ERG nor VEP showed any significant abnormalities,and no behavioral signs of visual disturbance were observed.These results indicate that DAPB and quinine directly damageretinal function and the decoloration of the tapetal funduscaused by EB is not directly related to retinal function. Inaddition, the procedure used in this study to record the ERGand VEP was found to be reliable for assessing the visual toxicityof drugs in conscious dogs.     

Analysis of Palatogenesis in the Mouse with Exencephaly Induced by Cadmium Chloride

ABSTRACT It has been revealed that exencephalic mouse embryos were resistant to cleft palate induction when they were exposed to several teratogens known as cleft palate inducing agents. In the present study, palatogenesis in exencephalic mouse embryos, which were not exposed to cleft palate inducing teratogens, was observed. A single dose of 6 mg CdCl₂/kg body weight was intraperitoneally injected into pregnant Jcl:ICR mice at day 7.5 of gestation (plug day = day 0). Embryos were dissected from uterus at day 13.5 to 15.5, and the secondary palate was observed with a dissecting microscope or a scanning electron microscope (SEM). Of live embryos, 71.5% had exencephaly. Palatal shelves of exencephalic embryos were elevated earlier than non-exencephalic embryos, and there seem to be two modes of palatal fusion in exencephalic embryos. (1) "Parallel-shape." The anterior part of shelves were elevated at day 13.5. Distance between the opposite medial edges of both shelves decreased at the posterior part, and this closing proceeded to the anterior part, where the shelves began to fuse. (2) "V-shape." The posterior part of palatal shelves became closer at day 14.0 or day 14.25. The medial edge of both shelves began to fuse at this part, and this fusion proceeded anteriorly. The anterior parts of the shelves were elevated, and the medial edge of the anterior shelves was fused independently. It is suggested that these alterations of palatogenesis in exencephalic embryos are related to inhibitive mechanism(s) against cleft palate induction. Key words : palate, neural tube defects, skull, mice, cadmium