• Journal of fish pathology
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• v.30 no.1
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• pp.11-24
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• 2017

The current investigation dealing with the causative agent of mass mortalities in cultured Oreochromis niloticus. The diseased fish showed external hemorrhage, unilateral and bilateral eye opacity, ended by blindness and fish death. The postmortem lesions revealed congested friable kidney and spleen, and liver has yellow nodules. Obtained isolates were identified as Aeromonas hydrophila (the causative agent of Motile Aeromonas Septicemia) and found to be highly pathogenic as they contained hemolysin virulence gene causing mortality reached to 100 and 70% in intraperitoneal and intramuscular infection. The prevalence of MAS was 80% among the surveyed O. niloticus. Blood and serum were collected from naturally diseased, intraperitoneal and intramuscular injected O. niloticus for hematological and biochemical examination. Similarly, gills, musculature, kidney, liver and spleen were collected for histopathological evaluation, and micropathomorphological analysis of spleen was done. Macrocytic hypochromic anemia was recorded in the intraperitoneal infection. Serum protein, albumin and globulin were decrease only in naturally diseased fish. Leucocytosis with heterophilia and lymphocytosis were observed in naturally diseased and intraperitoneal infected fish. There were severe degenerative changes and hemorrhagic necrosis in the examined tissues which were more obvious in intraperitoneal than intramuscular infection. Activation and proliferation of melanocytes macrophages centers with severe hemosiderosis were recorded in spleen of naturally diseased and experimentally infected fish.

• Clinical and Experimental Pediatrics
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• v.65 no.4
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• pp.182-187
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• 2022

We frequently encounter newborn infants with thrombocytosis in the neonatal intensive care unit. However, neonatal thrombocytosis is not yet fully understood. Thrombocytosis is more frequently identified in newborns and young infants, notably more often in those younger than 2 years than in older children or adults. The production of megakaryocytes (megakaryopoiesis) and platelets (thrombopoiesis) is mainly regulated by thrombopoietin (TPO). Increased TPO levels during infection or inflammation can stimulate megakaryopoiesis, resulting in thrombopoiesis. TPO concentrations are higher in newborn infants than in adults. Levels increase after birth, peak on the second day after birth, and start decreasing at 1 month of age. Initial platelet counts at birth increase with gestational age. Thus, preterm infants have lower initial platelet counts at birth than late-preterm or term infants. Postnatal thrombocytosis is more frequently observed in preterm infants than in term infants. A high TPO concentration and low TPO receptor expression on platelets leading to elevated plasma-free TPO, increased sensitivity of megakaryocyte precursor cells to TPO, a decreased red blood cell count, and immaturity of platelet regulation are speculated to induce thrombocytosis in preterm infants. Thrombocytosis in newborn infants is considered a reactive process (secondary thrombocytosis) following infection, acute/chronic inflammation, or anemia. Thrombocytosis in newborn infants is benign, resolves spontaneously, and, unlike in adults, is rarely associated with hemorrhagic and thromboembolic complications.

• The Korean Journal of Physiology
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• v.15 no.1
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• pp.9-18
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• 1981

For centuries, ginseng has been used for the therapeutic purpose in oriental herb medicine. Several studies have been conducted in the past to evaluate the effect of ginseng on erythropoiesis. However the results were controversial. We therefore attempted in the present studies to evaluate the effect of ginseng on the erythropoietic activity. In one series of experiments, the recovery pattern of peripheral blood(red cell count, hemoglobin content, hematocrit and reticulocyte count) was studied in posthemorrhagic anemic rabbits. After animals were maintained with normal(control group) or 1 gm% ginseng (experimental group) diet for 2 weeks, hemorrhagic anemia was induced by withdrawing blood equivalent to 25% of the total blood volume and then changes in peripheral blood were followed for following 30 days. In other series of experiments, we studied effect of ginseng on erythrokinetics using $^{59}Fe$. $^{59}Fe(10{\sim}40\;{\mu}Ci/animal)$ was injected intravenously after animals were fed with normal (control group) or 1 gm% ginseng(experimental group) diet for 2 weeks. And radioactivities in the blood compartments were measured at appropriate intervals for 15 days. Front these various erythrokinetic parameters were estimated. Results are summarized as follows: 1) Reticulocyte count was higher in the experimental group than in the control group after 2 weeks of administration of experimental diet. During the posthemorrhagic period, the reticulocyte count increased in both the control and experimental groups, but the increase appeared much earlier in the experimental group. 2) The posthemorrhagic recoveries of hematocrit, hemoglobin content and red cell count appeared to be faster in the experimental group as compaired with the control group. 3) The half life$(T_{1/2})$ of $^{59}Fe$ in the plasma was significantly(P<0.05) shorter in the experimental group(82.6 min, N=8) than in the control group(121 min, N=6). Plasma iron turnover (PIT) of the experimental group (1.78 mg/dl/24 hr.) was approximately 4 times greater than that of the control group(0.45 mg/dl/24 hr.). 4) The maximum red cell utilization(RC-U) was 82.1% in the experimental group ana 74.5% in the control group. Red cell iron turnover(RIT) of the experimental group(1.62 mg/dl/24 hr.) was slightly higher than that of the control group(0.35 mg/dl/24 hr). 5) Erythron turnover was significantly(p<0.05) greater in the experimental group(1.27 mg/dl/24 hr.) than in the control group(0.24 mg/dl/24 hr.). Marrow transit time of the experimental group(2.05 days) tended to he faster than that of the control group(2.84 days). These results suggest that the gingseng improves the recovery of posthemorrhagic anemia and stimulates the erythropoiesis in rabbits.

• Journal of Korean Neurosurgical Society
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• v.54 no.3
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• pp.164-174
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• 2013

Objective : The aim of this study was to determine 30-day mortality and 6-month functional recovery rates in spontaneous intracerebral hemorrhage (S-ICH) patients undergoing hemodialysis treatment for end-stage renal disease (ESRD), and to compare the outcomes of these patients and S-ICH patients without ESRD. Methods : The medical records of 1943 S-ICH patients from January 2000 to December 2011 were retrospectively analyzed with focus on demographic, radiological, and laboratory characteristics. Results : A total of 1558 supratentorial S-ICH patients were included in the present study and 102 (6.5%) were ESRD patients. The 30-day mortality of the S-ICH patients with ESRD was 53.9%, and 29.4% achieved good functional recovery at 6 months post-S-ICH. Multivariate analysis showed that age, Glasgow Coma Scale (GCS) score, pupillary abnormality, ventricular extension of hemorrhage, hemorrhagic volume, hematoma enlargement, anemia, and treatment modality were independently associated with 30-day mortality in S-ICH patients with ESRD (p<0.05), and that GCS score, volume of hemorrhage, conservative treatment, and shorter hemodialysis duration was independently associated with good functional recovery at 6 months post-S-ICH in patients with ESRD (p<0.05). Conclusion : This retrospective study showed worse outcome after S-ICH in patients with ESRD than those without ESRD; 30-day mortality was four times higher and the functional recovery rate was significantly lower in S-ICH patients with ESRD than in S-ICH patients without ESRD.

• Clinical and Experimental Pediatrics
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• v.57 no.2
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• pp.96-99
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• 2014

Hemolytic uremic syndrome (HUS) is one of the most common causes of acute renal failure in childhood and is primarily diagnosed in up to 4.5% of children who undergo chronic renal replacement therapy. Escherichia coli serotype O157:H7 is the predominant bacterial strain identified in patients with HUS; more than 100 types of Shiga toxin-producing enterohemorrhagic E. coli (EHEC) subtypes have also been isolated. The typical HUS manifestations are microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency. In typical HUS cases, more serious EHEC manifestations include severe hemorrhagic colitis, bowel necrosis and perforation, rectal prolapse, peritonitis, and intussusceptions. Colonic perforation, which has an incidence of 1%-2%, can be a fatal complication. In this study, we report a typical Shiga toxin-associated HUS case complicated by small intestinal perforation with refractory peritonitis that was possibly because of ischemic enteritis. Although the degree of renal damage is the main concern in HUS, extrarenal complications should also be considered in severe cases, as presented in our case.

• Journal of Microbiology and Biotechnology
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• v.28 no.9
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• pp.1413-1425
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• 2018

Shiga toxins (Stxs) are the main virulence factors expressed by the pathogenic Stx-producing bacteria, namely, Shigella dysenteriae serotype 1 and certain Escherichia coli strains. These bacteria cause widespread outbreaks of bloody diarrhea (hemorrhagic colitis) that in severe cases can progress to life-threatening systemic complications, including hemolytic uremic syndrome (HUS) characterized by the acute onset of microangiopathic hemolytic anemia and kidney dysfunction. Shiga toxicosis has a distinct pathogenesis and animal models of Stx-associated HUS have allowed us to investigate this. Since these models will also be useful for developing effective countermeasures to Stx-associated HUS, it is important to have clinically relevant animal models of this disease. Multiple studies over the last few decades have shown that mice injected with purified Stxs develop some of the pathophysiological features seen in HUS patients infected with the Stx-producing bacteria. These features are also efficiently recapitulated in a non-human primate model (baboons). In addition, rats, calves, chicks, piglets, and rabbits have been used as models to study symptoms of HUS that are characteristic of each animal. These models have been very useful for testing hypotheses about how Stx induces HUS and its neurological sequelae. In this review, we describe in detail the current knowledge about the most well-studied in vivo models of Stx-induced HUS; namely, those in mice, piglets, non-human primates, and rabbits. The aim of this review is to show how each human clinical outcome-mimicking animal model can serve as an experimental tool to promote our understanding of Stx-induced pathogenesis.

• Clinical and Experimental Pediatrics
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• v.50 no.10
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• pp.931-937
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• 2007

The hemolytic uremic syndrome (HUS) is a rare disease of microangiopathic hemolytic anemia, low platelet count and renal impairment. HUS usually occurs in young children after hemorrhagic colitis by shigatoxin-producing enterohemorrhagic E. coli (D+HUS). HUS is the most common cause of acute renal failure in infants and young children, and is a substantial cause of acute mortality and morbidity; however, renal function recovers in most of them. About 10% of children with HUS do not reveal preceding diarrheal illness, and is referred to as D- HUS or atypical HUS. Atypical HUS comprises a heterogeneous group of thrombomicroangiopathy (TMA) triggered by non-enteric infection, virus, drug, malignancies, transplantation, and other underlying medical condition. Emerging data indicate dysregulation of alternative complement pathway in atypical HUS, and genetic analyses have identified mutations of several regulatory genes; i.e. the fluid phase complement regulator Factor H (CFH), the integral membrane regulator membrane cofactor protein (MCP; CD46) and the serine protease Factor I (IF). The uncontrolled activation of the complement alternative pathway results in the excessive consumption of C3. Plasma exchange or plasma infusion is recommended for treatment of, and has dropped the mortality rate. However, overall prognosis is poor, and many patients succumb to end-stage renal disease. Clinical presentations, response to plasma therapy, and outcome after renal transplantation are influenced by the genotype of the complement regulators. Thrombotic thrombocytopenic purpura (TTP), another type of TMA, occurs mainly in adults as an acquired disease accompanied by fever, neurologic deficits and renal abnormalities. However, less frequent cases of congenital or hereditary TTP associated with ADAMTS-13 (a disintegrin and metalloprotease, with thrombospondin 1-like domains 13) gene mutations have been reported, also. Recent advances in molecular genetics better allow various HUS to be distinguished on the basis of their pathogenesis. The genetic analysis of HUS is important in defining the underlying etiology, predicting the genotype-related outcome and optimizing the management of the patients.

• Korean Journal of Poultry Science
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• v.7 no.2
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• pp.18-27
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• 1980

Infectious bursal disease, so called Gumboro disease, is found world-wide in areas of intensive poultry farming. The clinical signs of the disease are very indicative, but most infections occur unnoticed due to the age of infection of chicken as well as the degree of virulence of virus affected. Edematous and hemorrhagic lesions in BF at early course of infection and the complete atrophies of BF in later are the most characteristic. The infection is considered highly contagious by direct contact, by fecal material and by contaminated feed and water. The virus is also highly resistant in environment and belongs to Diploma virus with size of 55 to 60nm of Ribovirus group. IBDV grows in embryos, embryonic cells and BF of susceptible chickens. Immune-diffusion using agar gel is the method of a choice to determine IBDV infection in chickens. Maternal immunity is very effective in protecting chickens of critical age when IBDV infection severely damages the function of BF. Immunosuppressive effect of IBDV causes more production losses than direct effects of clinical disease of IBD. Inclusion body hepatitis, infectious anemia and gangrenous dermatitis syndrome are the disease associated with the immunosuppressive condition of chickens.