Liver size is an important component in the diagnosis and follow-up of diffuse liver disease when testing for liver disease using ultrasonography. However, difficulties lies in determining the presence of hepatomegaly and liver atrophy because the method used for measuring liver size differs from one examiner to another and there is no relevant standard based on body build. The present study aims to propose a more objective method for liver size measurement and a reference range based on body build. A total of 260 normal adults (130 males, 130 females) participated in the study. Ultrasonography was performed in all participants to measure the size of the right lobe, left lobe, quadrate lobe, and caudate lobe of liver. Based on Physique Index(PI), a value derived from multiplying weight(kg) by height($m^2$), size of physique was divided into three groups including Group I with PI<150, Group II with $150{\leq}PI{\leq}250$, and Group III with PI>250. Thus, mean liver size by PI and a reference range with 95% reliability were suggested. The superoinferior diameter of right lobe was $12.34{\pm}1.18cm$ in males and $11.07{\pm}0.93cm$ in females, and its reference range was 10.64~11.0cm for Group I, 11.78~12.12cm for Group II, and 13.02~13.84cm for Group III. The anteroposterior diameter(T) of left lobe was $5.93{\pm}1.09cm$ in males and $5.18{\pm}0.99cm$ in females, and its reference range was 4.77~5.17cm for Group I, 5.49~5.79cm for Group II, and 6.68~7.44cm for Group III. The transverse diameter was $3.51{\pm}0.60cm$ in male participants and $3.42{\pm}0.49cm$ in female participants and its reference range was 3.29~3.51cm for Group I, 3.36~3.55cm for Group II, and 3.52~4.0cm for Group III. The caudate lobe index was $11.65{\pm}2.88cm^2$ in males and $9.62{\pm}2.18cm^2$ in females and its reference range was $8.83{\sim}9.75cm^2$ for Group I, $10.62{\sim}11.47cm^2$ for Group II, and $11.89{\sim}14.26cm^2$ for Group III. As a basic measurement method of liver size, the present study suggests measuring the superoinferior diameter for right liver lobe, the anteroposterior diameter for left liver lobe, the transverse diameter for quadrate lobe, and the caudate lobe index for caudate lobe. It is expected that this method along with its relevant reference range can be used as useful indicators in determining hepatomegaly and liver atrophy upon the diagnosis and follow-up testing of diffuse liver disease.
Liver cirrhosis (LC) is defined as comprising diffuse fibrosis and regenerating nodules of the liver. The biochemical and anatomical dysfunction in LC results from both reduced liver cell number and portal vascular derangement. Although several studies have investigated dysregulated genes in cirrhotic nodules, little is known about the genes implicated in the pathophysiologic change of LC or about their relationship with the degree of decompensation. Here, we applied cDNA microarray analysis using 38 HBsAg-positive LC specimens to identify the genes dysregulated in HBV-associated LC and to evaluate their relation to disease severity. Among 1063 known cancer- and apoptosis-related genes, we identified 104 genes that were significantly up- (44) or down- (60) regulated in LC. Interestingly, this subset of 104 genes was characteristically correlated with the degree of decompensation, called the Pugh-Child classification (20 Pugh-Child A, 10 Pugh-Child B, and 8 Pugh-Child C). Patient samples from Pugh-Child C exhibited a distinct pattern of gene expression relative to those of Pugh-Child A and B. Especially in Pugh-Child C, genes encoding hepatic proteins and metabolizing enzymes were significantly down-regulated, while genes encoding various molecules related to cell replication were up-regulated. Our results suggest that subsets of genes in liver cells correspond to the pathophysiologic change of LC according to disease severity and possibly to hepatocarcinogenesis.
Transgenic mice were generated by microinjecting a plasmid DNA containing the SV40 (simian virus 40) large T antigen (Tag) gene fused with mouse albumin promoter/enhancer sequences into fertilized one-cell mouse embryos. Among eleven founder transgenic animals, four developed hepatocellular carcinoma, two showed kidney cancer and one developed skin and brain tumors. Three stable transgenic lines, #1-2, #1-6 and #1-11 were established. Members of the lines #1-6 and #1-11 reproducibly developed liver tumors by 8 to 10 weeks of age but did not exhibit any phenotypic changes in other tissues. Histological changes loading to liver tumor formation occurred with predictable kinetics and could be classified into three distinct stages; (a) newborn to 3 weeks of age, characterized by hyperplastic hepatocytes with reduced amounts of cytoplasm without any nuclear alterations, (b) between 4 to 8 weeks of age, characterized by diffuse liver cell dysplasia without observable tumor nodules, and (c) 9 weeks of age and thereafter, characterized by hepatocellular carcinomas in the background of extensive liver dysplasia. Metastasis to the lung from a liver carcinoma was observed in #1-11 founder animal. This transgenic mouse system displays similarities with human liver cancers in a number of aspects and provides a useful model for the study of molecular events involved in hepatocarcinogenesis.
The liver fibrosis is a disease we often see in clinical medicine, and the persistence and repeatition of inflammation and necrosis of liver cells continue for several years, and it is proceeded to cirrhosis. So decrease of death rate and prevalence rate by complications of cirrhosis and hepatocellular carcinoma is main task of clinical medicine by protection of chronic liver ailment patients from proceeding to cirrhosis and hepatocellular carcinoma. So this study tried to represent the ultrasonic image, blood test, the relationship with liver stiffness of diffuse liver ailment patients as numbers. This study was performed with patients from whom the image was taken by ultrasonic and 141 people who were treated by fibroscan, the basic data for blood test was obtained from the test results at the time when ultrasonic image and liver fibroscan was performed. The statistical analysis was performed by One-way analysis of variance(ANOVA) to verify difference between groups. The value of liver stiffness was increased in the order of normal, chronic liver disease and cirrhosis. As a results, ALT and Albumin have no statistical difference between object groups, and there are statistical differences in the results of ultrasonic decoding at age, AST, ALP, Bilirubin, PLT, PT, and kPa, and they are statistically meaningful(p<0.005). And the value of liver stiffness of chronic liver ailment was presented only as over 12.5kPa in other study, but it was represented as numbers for quantitative diagnosis by presenting average kPa threshold value according to disease in this study. And by presenting relationship of diagnosed results, it is considered that it could be used as first tool to diagnose chronic liver ailment patients according to their disease.
Liver functions in diffuse parenchymal liver disease such as cirrhosis of the liver depend largely on the effective hepatic blood flow rather than on the individual cell functions. Clinical methods of measuring the hepatic blood flow were developed recently by the application of colloidal disappearance rate. In order to correlate the radiogold disappearance rate to conventional biochemical liver function tests, 21 normal subjects and 80 cases of cirrhosis of the liver were studied with both methods. The results are summarized as following: 1. The validity of external counting method to measure the blood disappearance rate of colloidal radiogold was confirmed by in vitro counting of the serial blood samples. 2. The blood disappearance rate of collidal radiogold was essentially the same. as the liver uptake rate of colloidal radiogold in normal and cirrhotic subjects with various degrees of functional disturbance. And it seemed there was no serious extrahepatic removal of the colloidal radiogold. 3. The disappearance rate of colloidal radiogold was not significantly changed by the posture change, but was enhanced by ingestion of 500 ml of water. 4. The disappearance rate of colloidal radiogold was not influenced by single dose of Telepaque, while BSP retention was increased after Telepaque. 5. The mean disappearance half time of colloidal radiogold in normal subjects was $2.49{\pm}0.391$(S.D.) minutes. The mean normal disappearance rate constant (K value) was $0.285{\pm}0.0428$(S.D.)/minute. 6. The colloidal radiogold disappearance half time was abnormally prolonged (over 3.2 min.) in $87.7{\pm}3.68$(S.D.) % of cirrhotic subjects. 7. In patients of liver cirrhosis the blood disappearance rate of colloidal radiogold correlated well to serum albumin and globulin levels and BSP retention which were considered to reflect functions of hepatic parenchymal cells. There was, however, no correlation between colloidal disappearance rate and thymol turbidity test, serum glutamic pyruvic transaminase, and serm alkaline phosphatase activities. The latters were considered to be associated with the activity of liver disease.
Journal of the Korean Association of Oral and Maxillofacial Surgeons
/
v.33
no.6
/
pp.690-693
/
2007
Benign symmetric lipomatosis(BSL) is a lesion characterized by symmetrical and diffuse growth of adipose tissue. It is commonly found in the posterior neck or upper trunk, manifesting itself as an entity known as Madelung disease or Lanoid-Bensaude syndrome. Lipomatosis affecting the tongue is very unusual. The etiology of BSL is unknown, but It can be associated with alcoholism, liver dysfunction, hypothyroidism. Because of its diffuse histologic feature, complete resection of the lesion is often difficult. Seventy one years old male patient, whose chief complaint was multiple nodules of tongue was referred to our department. The lesion was diagnosed histopathologically as BSL and subsequently removed surgically. So we report this rare case of BSL with literature review.
This study was conducted to observe the severity of the disease and pathogenecity of Babesia gibsoni parasite on the splenectomized dogs(SPD) and nonsplenectomized(intact) dogs (NSPD) experimentally infected with B gibsoni. The average prepatent period was 4 days in the SPD and 8 days in the NSPD, respectively. Peak parasitaemia(PE) ranged from 26% to 34% of erythrocytes infected in the SPD and from 4% to 5% in the NSPD. Latent parasitaemia was still detectable 40 days as low as under 1.0% of erythrocytes infected after the initial parasitaemia in the SPD. Blood packed cell volume(PCV) decreased to as little as 6.4% to 6.9% in the SPD. The clinical signs were mild fever and anemia in the NSPD, remissions and exacervations of temperature, intermittent or spike-like increases of temperature, progressive polychromatophilic macrocytic anemia with anisocytosis, icterus, marked loss of appetite, rarely haemoglobinuria, and deep brown-yellowish urine in the SPD. Gross pathologic changes mainly involved slightly enlargement of liver and spleen in the NSPD and marked enlargement of liver in the SPD. Anatomic changes associated with the disease included diffuse periportal and centrilobular hephatitis, and membranoproliferative glomerulonephritis. Hyaline droplets, resulting protein metabolic alterations, were found in the convoluted ephithelium of the kidney. The density of lymphocytes within the liver sinusoids was markedly increased. Aggregates of large monocytes and macrophages were demonstrated in the centrilobular veins of the liver. The density of these cells in the centrilobular veins were greatest in the SPD. The forms of B gibsoni parasite found in the acute stage of SPD were large signet ring form, small signet ring form, pyriform, elongated form, comma form, head-phone form, oval form, peared form, racket-like form, amoeboid form, triangle form, quartered form, dot form, band form and multiple, and rosette form, et al. The severity of the disease and pathogenecity of B gibsoni parasite were mild in the NSPD but fatal in the SPD.
Monabati, Ahmad;Vahedi, Amir;Safaei, Akbar;Noori, Sadat;Mokhtari, Maral;Vahedi, Leila;Zamani, Mehdi
Asian Pacific Journal of Cancer Prevention
/
v.17
no.4
/
pp.2285-2289
/
2016
Background: Epstein-Barr virus (EBV) positive diffuse large B-cell lymphoma (DLBCL) of the elderly is an entity introduced in the latest WHO classification of lymphoid tumors and defined in patients older than 50 years without prior lymphoma or immunodeficiency. However, recently it has also been seen in patients under 50. There is thus debate as to whether these are separate entities. Materials and Methods: In this retrospective study, we analyzed de novo DLBCL admitted to our institute over a period of two years. Clinical data included age, sex, nodal and extranodal presentation. The results of an immunohistochemistry (IHC) panel were also reviewed. IHC findings were mainly used to sub-classify DLBCL as germinal center vs. non germinal center types. IHC for identification of LMP-1 (latent membrane protein) and in situ hybridization for detection of EBV-encoded RNA (EBER) was performed. EBV prevalence, clinical data and IHC findings were compared between patients under and over 50 years of age. Results: Out of 95 DLBCL, 11.6% were EBV positive (7.5% and 14.5% in the young and old groups). We did not find any significant differences in IHC subclasses and clinical data between EBV positive DLBCL (EBV+DLBCL) of young and old groups. Conclusions: EBV+DLBCL are not exclusive to patients older than 50 years. With regard to clinical data as well as IHC subclasses, no differences were evident between EBV+DLBCL of young and old groups. Our suggestion is to eliminate any cut off age for EBV+DLBCL.
Purpose: Gallbladder (GB) wall thickening can be found in various conditions unrelated to intrinsic GB disease. We investigated the predisposing etiologies and the outcome of acalculous GB wall thickening in children. Methods: We retrospectively analyzed 67 children with acalculous GB wall thickening who had visited our institute from June 2010 to June 2013. GB wall thickening was defined as a GB wall diameter > 3.5 mm on abdominal ultrasound examination or computed tomography. Underlying diseases associated with GB wall thickening, treatment, and outcomes were studied. Results: There were 36 boys and 31 girls (mean age, $8.5{\pm}4.8years$ [range, 7 months-16 years]). Systemic infection in 24 patients (35.8%), acute hepatitis in 18 (26.9%), systemic disease in 11 (16.4%), hemophagocytic lymphohistiocytosis in 4 (6.0%), acute pancreatitis in 3 (4.5%), and specific liver disease in 3 (4.5%) predisposed patients to GB wall thickening. Systemic infections were caused by bacteria in 10 patients (41.7%), viruses in 5 patients (20.8%), and fungi in 2 patients (8.3%). Systemic diseases observed were systemic lupus erythematosus in 2, drug-induced hypersensitivity in 2, congestive heart failure in 2, renal disorder in 2. Sixty-one patients (91.0%) received symptomatic treatments or treatment for underlying diseases. Five patients (7.5%) died from underlying diseases. Cholecystectomy was performed in 3 patients during treatment of the underlying disease. Conclusion: A wide range of extracholecystic conditions cause diffuse GB wall thickening that resolves spontaneously or with treatment of underlying diseases. Surgical treatments should be avoided if there are no definite clinical manifestations of cholecystitis.
Patients with lysosomal acid lipase (LAL) deficiency and glycogen storage disease (GSD) demonstrated hepatomegaly and dyslipidemia. In our case, a 6-year-old boy presented with hepatosplenomegaly. At 3 years of age, GSD had been diagnosed by liver biopsy at another hospital. He showed elevated serum liver enzymes and dyslipidemia. Liver biopsy revealed diffuse microvesicular fatty changes in hepatocytes, septal fibrosis and foamy macrophages. Ultrastructural examination demonstrated numerous lysosomes that contained lipid material and intracytoplasmic cholesterol clefts. A dried blood spot test revealed markedly decreased activity of LAL. LIPA gene sequencing identified the presence of a novel homozygous mutation (p.Thr177Ile). The patient's elevated liver enzymes and dyslipidemia improved with enzyme replacement therapy. This is the first report of a Korean child with LAL deficiency, and our findings suggest that this condition should be considered in the differential diagnosis of children with hepatosplenomegaly and dyslipidemia.
본 웹사이트에 게시된 이메일 주소가 전자우편 수집 프로그램이나
그 밖의 기술적 장치를 이용하여 무단으로 수집되는 것을 거부하며,
이를 위반시 정보통신망법에 의해 형사 처벌됨을 유념하시기 바랍니다.
[게시일 2004년 10월 1일]
이용약관
제 1 장 총칙
제 1 조 (목적)
이 이용약관은 KoreaScience 홈페이지(이하 “당 사이트”)에서 제공하는 인터넷 서비스(이하 '서비스')의 가입조건 및 이용에 관한 제반 사항과 기타 필요한 사항을 구체적으로 규정함을 목적으로 합니다.
제 2 조 (용어의 정의)
① "이용자"라 함은 당 사이트에 접속하여 이 약관에 따라 당 사이트가 제공하는 서비스를 받는 회원 및 비회원을
말합니다.
② "회원"이라 함은 서비스를 이용하기 위하여 당 사이트에 개인정보를 제공하여 아이디(ID)와 비밀번호를 부여
받은 자를 말합니다.
③ "회원 아이디(ID)"라 함은 회원의 식별 및 서비스 이용을 위하여 자신이 선정한 문자 및 숫자의 조합을
말합니다.
④ "비밀번호(패스워드)"라 함은 회원이 자신의 비밀보호를 위하여 선정한 문자 및 숫자의 조합을 말합니다.
제 3 조 (이용약관의 효력 및 변경)
① 이 약관은 당 사이트에 게시하거나 기타의 방법으로 회원에게 공지함으로써 효력이 발생합니다.
② 당 사이트는 이 약관을 개정할 경우에 적용일자 및 개정사유를 명시하여 현행 약관과 함께 당 사이트의
초기화면에 그 적용일자 7일 이전부터 적용일자 전일까지 공지합니다. 다만, 회원에게 불리하게 약관내용을
변경하는 경우에는 최소한 30일 이상의 사전 유예기간을 두고 공지합니다. 이 경우 당 사이트는 개정 전
내용과 개정 후 내용을 명확하게 비교하여 이용자가 알기 쉽도록 표시합니다.
제 4 조(약관 외 준칙)
① 이 약관은 당 사이트가 제공하는 서비스에 관한 이용안내와 함께 적용됩니다.
② 이 약관에 명시되지 아니한 사항은 관계법령의 규정이 적용됩니다.
제 2 장 이용계약의 체결
제 5 조 (이용계약의 성립 등)
① 이용계약은 이용고객이 당 사이트가 정한 약관에 「동의합니다」를 선택하고, 당 사이트가 정한
온라인신청양식을 작성하여 서비스 이용을 신청한 후, 당 사이트가 이를 승낙함으로써 성립합니다.
② 제1항의 승낙은 당 사이트가 제공하는 과학기술정보검색, 맞춤정보, 서지정보 등 다른 서비스의 이용승낙을
포함합니다.
제 6 조 (회원가입)
서비스를 이용하고자 하는 고객은 당 사이트에서 정한 회원가입양식에 개인정보를 기재하여 가입을 하여야 합니다.
제 7 조 (개인정보의 보호 및 사용)
당 사이트는 관계법령이 정하는 바에 따라 회원 등록정보를 포함한 회원의 개인정보를 보호하기 위해 노력합니다. 회원 개인정보의 보호 및 사용에 대해서는 관련법령 및 당 사이트의 개인정보 보호정책이 적용됩니다.
제 8 조 (이용 신청의 승낙과 제한)
① 당 사이트는 제6조의 규정에 의한 이용신청고객에 대하여 서비스 이용을 승낙합니다.
② 당 사이트는 아래사항에 해당하는 경우에 대해서 승낙하지 아니 합니다.
- 이용계약 신청서의 내용을 허위로 기재한 경우
- 기타 규정한 제반사항을 위반하며 신청하는 경우
제 9 조 (회원 ID 부여 및 변경 등)
① 당 사이트는 이용고객에 대하여 약관에 정하는 바에 따라 자신이 선정한 회원 ID를 부여합니다.
② 회원 ID는 원칙적으로 변경이 불가하며 부득이한 사유로 인하여 변경 하고자 하는 경우에는 해당 ID를
해지하고 재가입해야 합니다.
③ 기타 회원 개인정보 관리 및 변경 등에 관한 사항은 서비스별 안내에 정하는 바에 의합니다.
제 3 장 계약 당사자의 의무
제 10 조 (KISTI의 의무)
① 당 사이트는 이용고객이 희망한 서비스 제공 개시일에 특별한 사정이 없는 한 서비스를 이용할 수 있도록
하여야 합니다.
② 당 사이트는 개인정보 보호를 위해 보안시스템을 구축하며 개인정보 보호정책을 공시하고 준수합니다.
③ 당 사이트는 회원으로부터 제기되는 의견이나 불만이 정당하다고 객관적으로 인정될 경우에는 적절한 절차를
거쳐 즉시 처리하여야 합니다. 다만, 즉시 처리가 곤란한 경우는 회원에게 그 사유와 처리일정을 통보하여야
합니다.
제 11 조 (회원의 의무)
① 이용자는 회원가입 신청 또는 회원정보 변경 시 실명으로 모든 사항을 사실에 근거하여 작성하여야 하며,
허위 또는 타인의 정보를 등록할 경우 일체의 권리를 주장할 수 없습니다.
② 당 사이트가 관계법령 및 개인정보 보호정책에 의거하여 그 책임을 지는 경우를 제외하고 회원에게 부여된
ID의 비밀번호 관리소홀, 부정사용에 의하여 발생하는 모든 결과에 대한 책임은 회원에게 있습니다.
③ 회원은 당 사이트 및 제 3자의 지적 재산권을 침해해서는 안 됩니다.
제 4 장 서비스의 이용
제 12 조 (서비스 이용 시간)
① 서비스 이용은 당 사이트의 업무상 또는 기술상 특별한 지장이 없는 한 연중무휴, 1일 24시간 운영을
원칙으로 합니다. 단, 당 사이트는 시스템 정기점검, 증설 및 교체를 위해 당 사이트가 정한 날이나 시간에
서비스를 일시 중단할 수 있으며, 예정되어 있는 작업으로 인한 서비스 일시중단은 당 사이트 홈페이지를
통해 사전에 공지합니다.
② 당 사이트는 서비스를 특정범위로 분할하여 각 범위별로 이용가능시간을 별도로 지정할 수 있습니다. 다만
이 경우 그 내용을 공지합니다.
제 13 조 (홈페이지 저작권)
① NDSL에서 제공하는 모든 저작물의 저작권은 원저작자에게 있으며, KISTI는 복제/배포/전송권을 확보하고
있습니다.
② NDSL에서 제공하는 콘텐츠를 상업적 및 기타 영리목적으로 복제/배포/전송할 경우 사전에 KISTI의 허락을
받아야 합니다.
③ NDSL에서 제공하는 콘텐츠를 보도, 비평, 교육, 연구 등을 위하여 정당한 범위 안에서 공정한 관행에
합치되게 인용할 수 있습니다.
④ NDSL에서 제공하는 콘텐츠를 무단 복제, 전송, 배포 기타 저작권법에 위반되는 방법으로 이용할 경우
저작권법 제136조에 따라 5년 이하의 징역 또는 5천만 원 이하의 벌금에 처해질 수 있습니다.
제 14 조 (유료서비스)
① 당 사이트 및 협력기관이 정한 유료서비스(원문복사 등)는 별도로 정해진 바에 따르며, 변경사항은 시행 전에
당 사이트 홈페이지를 통하여 회원에게 공지합니다.
② 유료서비스를 이용하려는 회원은 정해진 요금체계에 따라 요금을 납부해야 합니다.
제 5 장 계약 해지 및 이용 제한
제 15 조 (계약 해지)
회원이 이용계약을 해지하고자 하는 때에는 [가입해지] 메뉴를 이용해 직접 해지해야 합니다.
제 16 조 (서비스 이용제한)
① 당 사이트는 회원이 서비스 이용내용에 있어서 본 약관 제 11조 내용을 위반하거나, 다음 각 호에 해당하는
경우 서비스 이용을 제한할 수 있습니다.
- 2년 이상 서비스를 이용한 적이 없는 경우
- 기타 정상적인 서비스 운영에 방해가 될 경우
② 상기 이용제한 규정에 따라 서비스를 이용하는 회원에게 서비스 이용에 대하여 별도 공지 없이 서비스 이용의
일시정지, 이용계약 해지 할 수 있습니다.
제 17 조 (전자우편주소 수집 금지)
회원은 전자우편주소 추출기 등을 이용하여 전자우편주소를 수집 또는 제3자에게 제공할 수 없습니다.
제 6 장 손해배상 및 기타사항
제 18 조 (손해배상)
당 사이트는 무료로 제공되는 서비스와 관련하여 회원에게 어떠한 손해가 발생하더라도 당 사이트가 고의 또는 과실로 인한 손해발생을 제외하고는 이에 대하여 책임을 부담하지 아니합니다.
제 19 조 (관할 법원)
서비스 이용으로 발생한 분쟁에 대해 소송이 제기되는 경우 민사 소송법상의 관할 법원에 제기합니다.
[부 칙]
1. (시행일) 이 약관은 2016년 9월 5일부터 적용되며, 종전 약관은 본 약관으로 대체되며, 개정된 약관의 적용일 이전 가입자도 개정된 약관의 적용을 받습니다.