Archaeological research since 2004 at the site of La Joya on the Gulf of Mexico
has revealed that earth was successfully used as a building material for monumental
architecture in the humid tropical coastal lowlands, an extremely adverse environment
with heavy summer rainfalls and winter hurricanes. It is one of the many earthen
sites of Central and Southern Veracruz, where pyramids, palaces, and ball courts
of a size equalling or surpassing contemporaneous stone constructions, were erected
during the first millennium AD. However, ignoring the value of these ancient cities,
many of these sites have been levelled for road fill or brickmaking. In the case of La
Joya, what started as a salvage excavation has become a pilot study in ancient earthen
architectural techniques and preservation experiments. This chapter focuses on
conservation strategies that have been developed at the site in order to maintain its
state of equilibrium. The data are useful both for earthen heritage conservation, as
for opening new possibilities for contemporary architecture in the humid tropics, for
which there has been limited interest in Mexico.
Cyclins, cyclin-dependent kinases (Cdks), and Cdk inhibitors (CdkIs) are frequently altered in human cancer. p18 INK4C , a member of the INK4 family of CdkIs, is a potential tumor-suppressor gene product. However, the expression of p18 INK4C in hepatocellular carcinoma (HCC) remains unknown. The aim of this study was to examine the expression of p18 INK4C in various liver diseases including HCC and to assess its clinical significance in HCC. To that end, we examined the expression of p18 INK4C by immunohistochemistry in various liver diseases, including 51 HCCs, and also studied the relationship between p18 INK4C expression, the phosphorylation of retinoblastoma protein (pRb), and the activity level of Cdk4 and Cdk6. Immunohistochemical analysis revealed the frequent loss of p18 INK4C expression in HCC, especially in poorly differentiated HCC. The loss of p18 INK4C expression was shown to be associated with a poor prognosis compared with that associated with p18 INK4C - positivity. Further, the kinase activity of Cdk4 was found to be higher in p18 INK4C -negative HCCs than in p18 INK4C - positive HCCs. However, the level of Cdk6 activity was similar in the 2 groups of HCCs. In p18 INK4C - positive HCCs, p18 INK4C dominantly interacted with Cdk4 rather than with Cdk6. pRb phosphorylated at serine(Ser) 780 was detected more frequently in p18 INK4C - negative than in p18 INK4C - positive HCCs. In conclusion , the loss of p18 INK4C expression may play a role in the differentiation and development of HCC through the up-regulation of Cdk4 activity. (Hepatology 2004;40:677-686.)
La arquitectura monumental del sitio arqueologico de La Joya, Medellin de Bravo, Veracruz, ha perdurado mil anos por algun tipo de estabilizante, el cual se interpreto en los trabajos anteriores como bitumen diluido en aceite vegetal. Recientemente, en el proceso de analisis quimico detallado aplicando el metodo para caracterizar crudos e identificar origen de bitumen arqueologico, se descubrio que las muestras de construccion prehispanica carecen de las fracciones mas pesadas, las de resinas (NSO) y asfaltenos. Por lo tanto, el estabilizante original no es bitumen (que contiene fracciones pesadas), sino son fracciones mas ligeras (aceite) de crudo. El muro experimental de adobes que se estabilizo en enero de 2013 solo con la pequena proporcion de aceite que solto el bitumen solido al calentarse en agua, ha resistido mas que el muro de control y los muros estabilizados con extractos vegetales. Esto indica la eficacia de proporciones muy bajas de las fracciones ligeras de crudo. Analisis geoquimicos combinados de cromatografia de gases acoplado a espectrometria de masas (CG-EM) y espectrometria de masas de isotopos estables (IRMS) estan en curso para confirmar el uso intencional de estas fracciones ligeras como estabilizante de tierra para la construccion prehispanica. Por otro lado, se continuan experimentos en el sitio que permiten fortalecer la investigacion sobre la tecnologia de arquitectura prehispanica, evaluando la efectividad de los estabilizantes, y al mismo tiempo examinar este material petrolifero como estrategia para la preservacion.
One hundred and forty-four urgent treatments for acute obstructive suppurative cholangitis (AOSC), acute obstructive cholangitis (AOC), or/and acute pancreatitis caused by impacted bile duct stones were performed for eight years from 1984 to 1991. The breakdown of these treatments are as follows. [table: see text] It was not easy to diagnose every severe case of AOSC. As a result, however, endoscopy was very effective both in diagnosis and treatment. Concerning patients with thinner bile duct, endoscopic drainage was useful than percutaneous drainage. We prefer ENBD to EST followed by basket extraction of bile duct stones in an emergency state. ENBD is a rather easy technique even for beginners of ERCP, and is less invasive. The life-saving effect of ENBD is not inferior to that of EST.
The adaptor molecule Shc is a proto-oncogene product, and it is known to be associated with cell proliferation. However, the role of Shc in the proliferation and regeneration of hepatocytes remains unknown. In the present study, we report that p46 Shc is specifically expressed in the nuclei of proliferative (or regenerative) hepatocytes, suggesting that p46 Shc protein plays a role in hepatocellular proliferation. The expression of Shc was analyzed in liver tissue after partial hepatectomy (PH) or sham operation in Wistar rats by using immunohistochemistry and/or Western blot analysis. In addition, the expression of various cell cycle-related proteins, such as Cdk4, cyclin D1, PCNA, and Cdk1 was analyzed in the tissues of regenerating rat liver. Furthermore, the tyrosine phosphorylation of Shc was studied in liver tissue after PH or sham operation by immunoprecipitation using a monoclonal phosphotyrosine antibody. Although the protein levels of p52 Shc were unchanged in liver tissues after PH or sham operation, tyrosine phosphorylation was detected only in the regenerating rat liver after PH. The levels of p46 Shc protein were markedly increased in liver tissues during the liver regenerative process. In contrast, p66 Shc was not detected in the liver tissues after PH or sham operation. Western blotting and immunohistochemistry showed that the main location of p46 Shc was in the nuclei of proliferating hepatocytes after PH. These data suggest that p46 Shc expressed in hepatocellular nuclei may be closely related to the proliferation of hepatocytes. Therefore, it is suggested that p46 Shc expressed in hepatocellular nuclei may be a useful marker for detecting hepatocytes with high proliferative activity.
It has been shown that a variety of cell cycle-related proteins play important roles in the process of carcinogenesis including hepatocarcinogenesis. In the present study, we evaluated mRNA and protein expression of G1 phase-related cell cycle molecules in the process of hepatocarcinogenesis, using Long-Evans Cinnamon (LEC) rats, an animal model of hepatocellular carcinoma (HCC). The expression of cyclin D1, cyclin-dependent kinase 4 (Cdk4) and Cdk6 was measured quantitatively by real-time polymerase chain reaction. Cyclin D1 mRNA expression was increased significantly in chronic hepatitis liver compared with normal liver, and then decreased in HCC and the surrounding precancerous liver of LEC rats. Levels of Cdk4 mRNA were increased significantly in HCC compared to precancerous and chronic hepatitis livers. In contrast, mRNA levels of Cdk6 did not change significantly during hepatocarcinogenesis. We also evaluated the protein levels of these G1 phase-related cell cycle molecules by Western blot analyses and confirmed similar results. Total amounts of retinoblastoma protein (pRb) in the liver did not change significantly in the process of hepatocarcinogenesis in LEC rats. However, levels of phosphorylated pRb were increased markedly in the process of hepatocarcinogenesis, and the highest in HCC compared to precancerous, chronic hepatitis and normal livers. These results indicate that cyclin D1 may be involved in the regeneration of hepatocytes rather than hepatocarcinogenesis, while Cdk4 but not Cdk6 may play an important role in the development of HCC.
A 18-year-old man was admitted urgently complaining dyspnea, cyanosis and chest pain. The chest x-ray film revealed simultaneous bilateral pneumothorax. Chest drains were inserted immediately to the both chest cavities. On the 3 rd hospital day, radical operation for spontaneous pneumothorax with synchronous bilateral thoracotomies were performed through both axillary incision. Postoperative course was uneventful. The patient was discharged on the 8 th day after operation.
Responses of the liver to chronic injury include inflammation, regeneration and fibrosis, which finally lead to cirrhosis. The cause of liver cirrhosis appears to be impaired proliferative capability of hepatocytes caused by continuous hepatic damage, and subsequent accumulation of extracellular matrix produced by hepatic stellate cells (HSCs). Epidermal growth factor (EGF) and transforming growth factor-beta1 (TGF-beta1) play a crucial role in hepatocyte proliferation and hepatofibrogenesis, respectively. However, sequential analyses of the intrahepatic expression of EGF and TGF-beta1 in the course of cirrhosis development have not been examined fully. In the present study, liver cirrhosis was produced in rats by intraperitoneal administration of dimethylnitrosamine (DMN), and intrahepatic mRNA expression levels of proliferating cell nuclear antigen (PCNA), EGF and TGF-beta1 were quantitatively estimated by a real-time reverse transcription-polymerase chain reaction method. Histological and semiquantitative densitometric examination of liver sections revealed that the accumulation of extracellular matrix components was increased according to the period of DMN treatment. Histological examination of liver sections of rats treated with DMN for 4 and 6 weeks revealed pre-cirrhosis and cirrhosis, respectively. Intrahepatic mRNA expression levels of PCNA and EGF correlated well. Expression levels of both molecules were increased significantly during the course of cirrhosis development, but decreased significantly at the time of complete cirrhosis manifestation. In contrast, intrahepatic TGF-beta1 expression was increased significantly according to the period of DMN treatment, and reached a peak at the time of cirrhosis manifestation. These results suggest that proliferative capability of hepatocytes was impaired by continuous liver damage due, in part, to the decrease of a hepatocyte mitogen EGF, and that increased intrahepatic TGF-beta1 activated HSCs to retrieve space lost by hepatocyte destruction, resulting in complete cirrhosis manifestation.
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