Ecotoxicological characterization of tannery wastewater in Dhaka, Bangladesh.

Tanning industries are one of the main economic activities in Bangladesh. It has been well documented that wastewater discharged from tanneries without appropriate treatment results in detrimental effects on the ecosystem. No ecotoxicity evaluation of any aquatic environment in Bangladesh has been conducted so far. In this study a battery of toxicity bioassays and chemical analysis were carried out from water samples obtained from three sampling points: upstream from discharging site on River Buriganga (S1), raw wastewater effluent (S2), and downstream the discharging sluice gate (S3), in the Hazaribagh tannery area of Dhaka City, Bangladesh. While S1 and S3 water samples did not show significant toxicity in the bioassays tested, S2 exhibited high acute toxicity to the bacterium Vibrio fischeri (15-min Microtox test, EC50 = 9.8%), the higher plant Lactuca sativa (5-day root elongation inhibition test, EC50 = 14.2%), and the microcrustacean Daphnia magna (24-hour mobility test, EC50 = 31.5%). The results suggested that the raw wastewater effluent had detrimental effects on broad spectrum of organisms in the aquatic ecosystem and bacterium was the most sensitive. The chemical analysis revealed that sample S2 contained an extremely high concentration of chromium (47 g l(-1)). Additionally microbiological analysis indicated that the sampling area is impacted by fecal pollution, increasing the environmental health risk for its inhabitants.

Large complex formation of the inhibitor of caspase-activated DNase.

Inhibitor of caspase-activated DNase (ICAD) is required for correctly folding of CAD and inhibits nuclease activity of CAD in non-apoptotic cells. From proteomic analysis of the ICAD binding proteins, we revealed that over-expressed flag-ICAD bound other ICAD molecules. Purified recombinant ICAD protein showed three bands, 66 KDa, 132 KDa and 450 KDa, by native-PAGE. ICAD fused with glutathione-S-transferase (GST) was immunoprecipitated with anti-flag antibody from Jurkat cell lysates cotransfected with ICAD fused with either GST or flag expression vectors. When purified recombinant ICAD protein was separated by gel chromatography, the molecular weight of ICAD was detected at approximately 440 and 45 K. ICAD in extracts of wild type Jurkat cells also existed at approximately 440 and 45 K as measured by gel chromatography; so that fractions of CAD coincided with fractions of approximately 440 K of ICAD. These results indicate that ICAD and/or CAD appeared to form large complexes in Jurkat cells.

Deletion 7p in gastric MALT lymphoma.

Deletion of the long arm of chromosome 7 has been related to loss of tumor suppressor genes which may constitute a primary step of carcinogenesis in many kinds of malignancies, including low-grade B-cell lymphoma. However, deletion of the short arm of chromosome 7, del(7p), in low-grade B-cell lymphoma has not been reported. Here, we report a case of gastric MALT lymphoma with the chromosome aberration del(7p) which progressed in spite of eradication of Helicobactor pylori. Deletion 7p may represent a new karyotypic change that is possibly related to autonomous growth of MALT lymphoma.

Sjögren's syndrome complicated with autoimmune hepatitis and antiphospholipid antibody syndrome.

A 56-year-old Japanese female simultaneously developed thrombocytopenia, sicca symptoms, and an elevation of transaminase. Antiphospholipid antibodies were detected in her serum. The presence of anti-SS-A antibodies in the serum and sialectasis, disclosed by sialography, suggested the presence of primary Sjogren's syndrome (SjS). The laboratory data and the biopsy of the liver showed compatible findings with autoimmune hepatitis (AIH). Thrombocytopenia and liver dysfunction satisfactorily responded to corticosteroid. To our knowledge, this is the first reported case of SjS with AIH and antiphospholipid antibody syndrome (APAS). Analysis of serum cytokine levels showed a predominance of Th0-Th1 response, which is not compatible with AIH, in this complicated autoimmune state.

Influences of The Great Hanshin-Awaji Earthquake on glycemic control in diabetic patients.

We investigated influences on glycemic control in 177 diabetic patients after The Great Hanshin-Awaji Earthquake which occurred on January 17, 1995. Changes in serum HbA(1c) level were studied according to the worsen rate of dietary and living conditions. A significant temporary increase in the mean value of HbA(1c) level was found after the earthquake (8.34 +/- 2.07% in March, 1995 vs. 7.74 +/- 1.82% in December, 1994, P < 0.01). Ninety nine of them showed more than 0.5% in the rate of increase. Multiple regression analysis was applied to the following factors: inappropriate diet, discontinuation of drug uptake, reduction of exercise, destruction of house, long stay at shelter, sex, age, and pre-earthquake therapy. Among them, inappropriate diet demonstrated the highest partial regression coefficient to raise the mean value of the HbA(1c) level. The increased level of HbA(1c) declined gradually to the pre-earthquake level in September, 1995. This study emphasizes the importance of appropriate diet for diabetic patients during a natural disaster. To fulfil it, medical staff have to educate diabetic patients of their disorders tediously in ordinary time. In addition, it seems quite useful to supply a medical information card and a small medical bag containing essential drugs to each patient.

Idiopathic chronic calcifying pancreatitis with diabetes mellitus. Analysis of pancreatic stone protein gene.

We present a case of a 27-year-old female suffering from chronic calcifying pancreatitis with diabetes mellitus. Radiographic examinations and exocrine pancreatic function tests revealed considerable dilatation of pancreatic ducts with large intraductal calculi and exocrine pancreatic insufficiency, respectively. Recent literature indicates that a decrease in the activity of pancreatic stone protein (PSP), which inhibits CaCO3 crystal formation in pancreatic juice, is closely related to the development of chronic calcifying pancreatitis. The patient had no apparent cause or family history of pancreatitis. We therefore investigated the possibility that alterations in the PSP gene might explain the chronic pancreatitis seen in this patient. Six exons of the PSP gene amplified by polymerase chain reaction were directly sequenced, but there was no apparent base mutation observed. Furthermore, Southern blot analysis revealed neither rearrangement nor deletion of the PSP gene in the genomic DNA of this case. However, this genetic approach will be useful for future study of the etiology of hereditary pancreatitis.

[Malignancies in patients with sarcoidosis].

We evaluated the occurrence and type of malignant tumors in 148 patients with sarcoidosis followed at the Okayama University Hospital. Nine patients had malignancies; in 2 of 9 patients the development of malignancy preceded that of sarcoidosis, and one patient presented with sarcoidosis and malignancy at the same time. Six patients developed six types of malignancy following the development sarcoidosis; one case each of stomach cancer, lung cancer, breast cancer, thyroid cancer, testicular tumor, laryngeal cancer, and chronic lymphocytic leukemia. There was no significant difference between sexes (3 males and 3 females). The mean age of the cancer group at the onset of sarcoidosis was 56 years, which was significantly higher (p less than 0.05) than that of the control group. In these 6 patients, the mean interval from onset of sarcoidosis to detection of cancer was 11.7 years (range 1.5 to 30.2 years). The relative risk of malignancy was calculated based on the data for 148 patients with sarcoidosis with a total of 1371 person-years. The expected incidences of cancer for all sites and specific sites were estimated by applying age- and sex-adjusted person-years. The observed incidence of cancer was significantly (p less than 0.05) greater than the expected incidence for thyroid cancer, laryngeal cancer, and leukemia. No significant difference in incidence was found for all sites or for the other sites of cancer. The increased cancer incidence in sarcoidosis may be secondary to immunological abnormalities associated with this disease.

[Release of interleukin-6 by alveolar macrophages in patients with sarcoidosis].

The supernatants from cultures of alveolar macrophages from 12 patients with sarcoidosis and 7 control subjects were assayed for interleukin-6 (IL-6) using an ELISA system. IL-6 was detectable without a stimulant in supernatants from all subjects with sarcoidosis and controls. However, the supernatants from 4 of 12 untreated patients with sarcoidosis contained significantly greater amounts of IL-6. When macrophages were stimulated by Propionibacterium acnes (P. acnes), the mean level of IL-6 in the supernatant of patients with sarcoidosis was 5.18 +/- 1.46 ng/ml, which was significantly higher than in controls (3.34 +/- 0.39) (p less than 0.05). Furthermore, in patients with sarcoidosis, the mean level of IL-6 in the supernatant was significantly correlated with the percentage of lymphocytes in bronchoalveolar lavage fluid (p less than 0.05), the level of interleukin-1 released by alveolar macrophages stimulated by P. acnes (p less than 0.05), and the phagocytic index of alveolar macrophages (p less than 0.05). The large amount of IL-6 in the supernatant after stimulation by LPS was measured in patients with sarcoidosis (24.49 +/- 13.36) and in controls (12.4 +/- 8.53), and there was no significant difference between patients with sarcoidosis and controls. Small amounts of IL-6 were detectable in bronchoalveolar fluid from only 2 of 26 patients with sarcoidosis; however, it was detected in none of 15 controls. It is suggested that the enhancement of IL-6 release by alveolar macrophages has a role in the activation of immune effector cells at sites of sarcoidosis.

Clinical features of 125 patients with sarcoidosis: Okayama University Hospital review of a recent 10-year period.

Clinical features were studied in 125 patients with sarcoidosis (72 females and 53 males) diagnosed at Okayama University Hospital during a recent 10-year period. The age distribution had two peaks in patients in their 20s and the 50s. Over half of the patients were detected at health screening check and were asymptomatic, while the remaining were symptomatic. Twelve patients were in stage 0, 41 were in stage I, 54 were in stage II, 16 were in stage III, and 2 were in stage IV according to the chest x-ray findings. Serum angiotensin converting enzyme levels and serum lysozyme levels were elevated in 60% and 76% of the patients, respectively. The bronchoalveolar lavage fluid showed lymphocytosis, especially of helper T-cells. The clinical features of sarcoidosis appear to depend on the duration of the disease.

Effects of fluorine emission on agricultural products surrounding an aluminum factory.

The F concentrations of precipitate dust, agricultural products, and fingernail and hair at the surrounding Al factory were investigated. The F content of dust ranged from 15400 to 42500 micrograms/g dry weight, 190,000 to 380,000 micrograms/g Al. Rice grain contained about 3.4 times more F than that in the control area, but some kinds of agricultural products, egg plants (S. melongena L.), mulberry plants (M. japonica Bailey non Sieb.), and soy beans (G. max (L.) Merrill) were almost equal to that of controls. Also, the high F concentration in the hair and nails of some workers was affected by available F contents in the emission from the factory as well as food and water surrounding the aluminum factory compared with those of control area.

[Structural characterization of the somatostatin receptors on rat cerebrocortical membranes].

We characterized structurally the receptors for somatostatin in rat cerebral cortex by affinity labeling with [125I-Tyr1] somatostatin. [125I-Tyr1] somatostatin was cross-linked to cerebrocortical membranes using photoreactive cross-linker: N-5-azido-2-nitrobenzoyloxy-succinimide. Analysis by autoradiography revealed a broad band centered at Mr = 72,000 in the presence or absence of dithiothreitol. Affinity labeling of and specific [125I-Tyr1] somatostatin binding to cerebrocortical membranes were decreased similarly by adding unlabeled somatostatin or nonhydrolyzable guanine nucleotide analogue, guanyl-5'-yl imidodiphosphate, in a dose dependent manner. The pretreatment of cerebrocortical membranes with islet activating protein resulted in a decrease in subsequent affinity labeling of the protein. The cross-linked protein could be solubilized with Zwittergent 3-12 and poorly with digitonin, triton X-100 and NP-40. When exposed to agarose-coupled lectins, the solubilized labeled protein was absorbed to wheat germ agglutinin, partially to ricin communis-II, and not to concanavalin A or lentil lectin. The Mr = 72,000 protein bound to wheat germ agglutinin-agarose was eluted with not only N,N',N"-triacetylchitotriose but also N-acetylglucosamine. These results suggest that somatostatin receptors on cerebrocortical membranes are a monomeric glycoprotein with a Mr = 70,000 containing no disulfide-linked binding subunit, which is coupled to islet activating protein-sensitive guanine nucleotide regulatory protein.

[Ultrasonographic analysis of splenomegaly in patients with sarcoidosis].

Thirty seven patients with sarcoidosis were examined using ultrasound (US) to determine the size of the spleen. A Spleen Index (SI) was employed to evaluate splenomegaly and the SI was calculated using long (a) and short (b) dimensions on the sectional splenotomogram (SI = a x b). In 21 (57%) of these patients the spleen was judged ultrasonographically to be enlarged (SI 30), but in only 3 was it palpable. The clinical records of patients with and without splenomegaly detected by US were compared. There were no differences between patients with or without splenomegaly in hematologic findings (peripheral blood and bone marrow) or blood chemistry; furthermore no patients with hypersplenism were seen. In immunological parameters, the serum immunosuppressive acid protein level was significantly (p less than 0.05) higher in patients with splenomegaly than in those without splenomegaly; however, there were no differences in serum angiotenins converting enzyme activity, serum lysozyme level, PPD skin test or bronchoalveolar lavage fluid analysis. The patients with splenomegaly had significantly higher evidence of increased uptake of 67-Gallium in lung fields and positive lung infiltrates in chest X-ray than those without splenomegaly (p less than 0.01, p less than 0.05). These data suggest that ultrasound is a promising diagnostic tool for the assessment of the size of the spleen and is useful to detect disease activity and extent of disease in sarcoidosis. Patients with sarcoidosis who had splenomegaly had more disseminated disease, especially pulmonary parenchymal disease, than did those without splenomegaly.

The critical levels and the maximum metal uptake for wheat and rice plants when applying metal oxides to soil.

Wheat is more sensitive to CdO and ZnO compared with rice plant. The yield of wheat decreased by 30% in the presence of 30 ppm Cd, but that of rice plants by only 8%. The critical levels of meal uptake by wheat and rice plants for applying metal oxides to soil (CdO, ZnO, PbO) were determined. The highest concentration obtained for wheat grain was 141 micrograms/g Cd at the Cd 10,000 ppm in soil. This value is higher than the value of 4.97 micrograms/g for unpolished rice and higher than any other we have seen in the reports for treatment with CdO. Also, concentration of more than 1.0 micrograms/g Cd in wheat was observed at 5 pm Cd, while similar concentrations for rice plants were observed at 30 ppm Cd in soil.

[Coupling of inhibitory GTP binding protein to somatostatin receptors on rat cerebrocortical membranes].

We studied the interaction between somatostatin receptors and inhibitory GTP binding protein in rat cerebrocortical membranes. Guanine nucleotides reduced [125I-Tyr1] somatostatin binding to cerebrocortical membranes in a dose-dependent manner with rank order of potency being guanyl-5'-yl-imidodiphosphate (Gpp(NH)p) greater than GTP greater than GMP. Maximum reduction of the binding to 32% of control was observed in the presence of 10(-5) M Gpp(NH)p. Scatchard analysis of the labeled somatostatin binding revealed that the decrease in the binding by Gpp(NH)p was due to the decrease in the binding affinity for somatostatin. Divalent cations, such as Mg++, Mn++, and Ca++, caused an increase in labeled somatostatin binding to membranes with the maximum binding observed at a concentration of 10, 10, 1 mM, respectively. However, Na+ decreased a labeled somatostatin binding in a dose-dependent manner, and half maximum inhibition of the binding was observed at 10 mM Na+. Moreover, Gpp(NH)p and Na+ lowered labeled somatostatin binding in an additive fashion. When cerebrocortical membranes were treated at 37 degrees C for 40 min with various concentrations of Islet-Activating-Protein (IAP), which had been preactivated with dithiothreitol, subsequent labeled somatostatin binding to the membranes was decreased in a dose-dependent manner. 30 micrograms/ml IAP treatment caused a decrease in the binding to 50% of control, which was characterized by the decreased binding affinity without a significant change in the binding capacity. Furthermore, exposure of IAP plus NAD to cerebrocortical membranes caused ADP-ribosylation of a membrane protein with Mr = 41,000 on autoradiogram. Such an IAP treatment of cerebrocortical membranes abolished the inhibitory effect of somatostatin on vasoactive intestinal peptide-stimulated increase in adenylate cyclase activity. These results suggest that somatostatin receptors in the brain couple to inhibitory GTP binding protein, which mediates adenylate cyclase inhibition by somatostatin.

[Characterization of cholecystokinin receptors in gastric chief cells--effect of CCK analogs and CCK receptor antagonists on chief cells].

In isolated guinea pig gastric chief cells, gastrin-I and cholecystokinin-hexapeptide (CCK-4) stimulated pepsinogen release. However, the efficacies of these two peptide were 51% of that observed with CCK-octapeptide (CCK8). CR1409 and L-364718, both of which are new CCK receptor antagonists in pancreatic acinar cells, also inhibited 10(-8) M CCK8-stimulated pepsinogen release with a half-maximal inhibitory concentration (IC50) observed at 3 x 10(-9) M, respectively. The dose response curve to CCK8 for pepsinogen release shifted to the right in the presence of CR1409 or L-364718. The IC50 of these two antagonists for the CCK8-stimulated increase in cytosolic Ca2+ concentration monitored by Fura-2 were equal to those for CCK8-stimulated pepsinogen release. By contrast, the IC50 of dibutyryl cyclic GMP, a well-known CCK receptor antagonist, for CCK8-stimulated pepsinogen release was less than that for CCK8-stimulated increase in cytosolic Ca2+ concentration. Results suggested that CCK receptors in gastric chief cells are unique and may be different from CCK receptors in other tissues previously reported.

[A case of chronic adult T-cell leukemia benefited by small doses of MEPP].

A 59-year-old man diagnosed as a chronic ATL with cutaneous invasion, was treated with small doses of CPM, ADM, VDS and PSL regimens according to CHOP. The treatment was successful and achieved PR at the first stage of the therapy, but it became refractory later. He was then treated with small MEPP (MXT, VP-16, CDDP and PSL) as the salvage therapy for non-Hodgkin's lymphoma. This case suggested that small MEPP might be a useful combination chemotherapy for ATL.

G protein in stimulation of PI hydrolysis by CCK in isolated rat pancreatic acinar cells.

To clarify the possible role of a guanine nucleotide-binding protein (G protein) in the signal transducing system activated by cholecystokinin (CCK), actions of CCK on rat pancreatic acini were compared with those of fluoride, a well-known activator of stimulatory (Gs) or inhibitory (Gi) G protein. When acini were incubated with increasing concentrations of either CCK-octapeptide (CCK8) or NaF, a maximal stimulation of amylase release from acini occurred at 100 pM CCK8 or 10 mM NaF, respectively; this secretory rate decreased as CCK8 or NaF concentration was increased. NaF caused an increased in cytoplasmic Ca2+ concentration from the internal Ca2+ store and stimulated accumulation of inositol phosphates in acini, as observed with CCK. However, NaF-stimulated Ca2+ mobilization had a lag period before detectable stimulation and was potentiated by AlCl3. These stimulatory effects of NaF appeared to be independent of cellular adenosine 3',5'-cyclic monophosphate (cAMP). Pretreatment with cholera toxin or pertussis toxin did not affect CCK8- or NaF-induced inositol phosphate accumulation or Ca2+ mobilization. 5'-Guanylimidodiphosphate activated the generation of inositol phosphates in the [3H]inositol-labeled pancreatic acinar cell membrane preparation, with half-maximal and maximal stimulation at 1 and 10 microM, respectively. Furthermore, the effects of submaximal CCK concentrations on inositol phosphate accumulation in membranes were markedly potentiated in the presence of 100 microM GTP, which alone was ineffective. Combined findings of the present study strongly suggest that pancreatic CCK receptors are probably coupled to the activation of polyphosphoinositide (PI) breakdown by a G protein, which appears to be fluoride sensitive but is other than Gs- or Gi-like protein.

Somatostatin receptors on rat cerebrocortical membranes. Structural characterization of somatostatin-14 and somatostatin-28 receptors and comparison with pancreatic type receptors.

Somatostatin binding and cross-linking to its receptors on rat cerebrocortical membranes were characterized with [125I-Tyr1]somatostatin-14 and [125I-Leu8, D-Trp22, Tyr25]somatostatin-28. When [125I-Tyr1]somatostatin-14 was cross-linked to its receptors with the photoreactive cross-linker, N-(5-azido-2-nitrobenzoyloxy)succinimide, the hormone was specifically associated with a Mr = 72,000 protein band in the presence or absence of reducing agents. Affinity labeling of the Mr = 72,000 protein band was decreased with increasing concentrations of unlabeled somatostatin-14 and nonhydrolyzable guanine nucleotide analog, guanyl-5'-yl imidodiphosphate (Gpp(NH)p). Pretreatment of cerebrocortical membranes with islet-activating protein resulted in a decrease in subsequent labeled somatostatin-14 binding and affinity-labeling of the protein and abolished an inhibitory effect of somatostatin-14 on vasoactive intestinal peptide-stimulated increase in adenylate cyclase activity. When the affinity-labeled protein was solubilized with Zwittergent 3-12 and adsorbed to wheat germ agglutinin-agarose, it was eluted by N-acetylglucosamine. [125I-Leu8, D-Trp22, Tyr25]somatostatin-28 cross-linking to cerebrocortical and pancreatic membranes with the same photoreactive agent revealed specifically labeled protein bands of a Mr = 74,000 in cerebrocortical membranes and a Mr = 94,000 in pancreatic membranes, respectively. These results suggest that: 1) somatostatin receptor on cerebrocortical membranes is a monomeric glycoprotein with a Mr = 70,000 binding subunit, coupled to guanine nucleotide regulatory protein, and 2) the Mr = 70,000 protein may be a common receptor for somatostatin-28 and somatostatin-14 and is distinct from a common pancreatic type receptor.