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was fixed in the distal common bileduct (proximal to the ampulla to avoid duodenal reflux and cholangitis). The tube was also secured at the point of exit from the liver. Intraoperative X-rays confirmed the accurate position of the tube with adequate flow from the dilated ducts within the liver to the common bileduct. The proximal end of the tube was plugged and passed through the muscle and fascia to be secured in a subcutaneous pocket. The tube was readily palpable under the skin. All 4 patients are at home and free of jaundice though the tube dislodged and was replaced with a percutaneous drain in one patient. This technique offers benefits. As an alternative to the U-tube, there are no external devices which require daily management and may cause both psychological and physical discomfort. Exogenous infection should not occur. The lumen of the tube is larger than that of most current endoprostheses and may be less prone to blockage. However, should jaundice recur, the tube is readily accessible beneath the skin and can be brought to the surface by a minor procedure to be cleaned by a flexible bronchoscope brush or replaced over a guidewire.7 This technique has a role in a clearly defined group of patients with tumours found to be non-resectable at laparotomy. Current investigations of the preoperative assessment of cholangiocarcinoma should allow delineation of cases which are neither resectable nor amenable to internal drainage by bypass and which may be best treated by percutaneously placed endoprostheses or exo-endoprostheses.

A double layer agar technique was used to investigate the proliferative state of granulocytic progenitor cells (Colony Forming Units in Culture; CFUc) in human peripheral blood and bone marrow. The sensitivity of the progenitor cells to the Sphase specific agent, hydroxyurea, was used as an index of the proportion of cells engaged in DNA synthesis. In the presence of low concentrations of colony stimulating factor (CSF) the CFUc were found to be virtually insensitive to the drug. However, when cultured in the presence of increasing concentrations of C S F the proportion of CFUc apparently killed by hydroxyurea increased to a maximum of 23% for those cells in the blood and 39% for those in the marrow. The results indicate that CFUc which are slowly proliferating are sensitive to low concentrations of CSF. In contrast, those CFUc which are proliferating more rapidly require high concentrations of CSF before they will form colonies in culture. A model has been devised which suggests that as CFUc mature, their cell cycle time shortens and their sensitivity to CSF decreases.

Phagocytosing, but not resting, neutrophils normally release an inhibitor of in-vitro granulopoiesis which suppresses the production or release of colony-stimulating factor by monocytes and macrophages. Neutrophils from 12 patients with chronic granulocytic leukaemia (CGL) were found to contain the inhibitor, but in 11 of the 12 patients there was failure to release significant amounts during phagocytosis. It is suggested that such a defect in the feedback control of granulopoiesis could lead to the progressive inappropriate accumulation of morphologically normal granulocytes, as seen in CGL.

We investigate the viability of collecting demonstrations, for learning robot control, in Virtual Reality (VR). If acceptable demonstrations can be collected offline using VR, problems with affecting the production line can be avoided and large amounts of realistic data from the actual production environment can be used. We show that the relatively low detail data that can be captured from the production line using a RGB-D camera provides sufficient information for an expert to perform acceptable demonstrations in Virtual-Reality. However, performance is not yet on par with what can be achieved through real world observations. We propose several future improvements that will help close the gap.

Late sowing of wheat in autumn due to environmental conditions or late harvesting of cotton crop results in substantial yield loss. It may be attributed to non-fulfillment of chilling requirements. The present study was conducted to identify the chilling requirement of autumn sown cultivars of wheat. Effect of chilling treatment (measured in vernalization days (VDs)) on seven wheat cultivars (five Pakistani and two American) was observed by exposing the seedlings to 6°C for 7, 14, 21, 28 and 35 days that is 6.72, 13.44, 20.16, 26.86 and 33.60 VDs. Seedlings which acted as control were not subjected to chilling treatment. All spring type wheat cultivars headed irrespective of their chilling treatment but increase in VDs, enhanced days to heading. Winter type wheat "Caldwell" did not show heading which indicated its high VDs requirement. Chilling treatment also affected grain yield of all cultivars. Sehar-06 and Marquillo demonstrated highest yields at 6.72 VDs while GA-02, Inqilab-91, Chakwal-50 and Freed-06 manifested highest yields at 13.44 VDs. The results of the experiment revealed that heading time and grain yield of all spring type wheat cultivars is affected by chilling treatments. Depending upon the response of the cultivars and available VDs calculated from temperature data of last 20 years. It is suggested that GA-02, Inqilab-91, Chakwal-50 and Fareed-06 must be sown in mid December while Sehar-06 can be sown in the start of January to meet their chilling requirement under field conditions without substantial yield reduction.

The inactivation of ribosomal protein S6 kinase 1 (S6K1) recapitulates aspects of caloric restriction and mTORC1 inhibition to achieve prolonged longevity in invertebrate and mouse models. In addition to delaying normative aging, inhibition of mTORC1 extends the shortened lifespan of yeast, fly, and mouse models with severe mitochondrial disease. Here we tested whether disruption of S6K1 can recapitulate the beneficial effects of mTORC1 inhibition in the Ndufs4 knockout (NKO) mouse model of Leigh Syndrome caused by Complex I deficiency. These NKO mice develop profound neurodegeneration resulting in brain lesions and death around 50-60 days of age. Our results show that liver-specific, as well as whole body, S6K1 deletion modestly prolongs survival and delays onset of neurological symptoms in NKO mice. In contrast, we observed no survival benefit in NKO mice specifically disrupted for S6K1 in neurons or adipocytes. Body weight was reduced in WT mice upon disruption of S6K1 in adipocytes or whole body, but not altered when S6K1 was disrupted only in neurons or liver. Taken together, these data indicate that decreased S6K1 activity in liver is sufficient to delay the neurological and survival defects caused by deficiency of Complex I and suggest that mTOR signaling can modulate mitochondrial disease and metabolism via cell non-autonomous mechanisms.

The inactivation of ribosomal protein S6 kinase 1 (S6K1) recapitulates aspects of caloric restriction and mTORC1 inhibition to achieve prolonged longevity in invertebrate and mouse models. In addition to delaying normative aging, inhibition of mTORC1 extends the shortened lifespan of yeast, fly, and mouse models with severe mitochondrial disease. Here we tested whether disruption of S6K1 can recapitulate the beneficial effects of mTORC1 inhibition in the Ndufs4 knockout (NKO) mouse model of Leigh Syndrome caused by Complex I deficiency. These NKO mice develop profound neurodegeneration resulting in brain lesions and death around 50-60 days of age. Our results show that liver-specific, as well as whole body, S6K1 deletion modestly prolongs survival and delays onset of neurological symptoms in NKO mice. In contrast, we observed no survival benefit in NKO mice specifically disrupted for S6K1 in neurons or adipocytes. Body weight was reduced in WT mice upon disruption of S6K1 in adipocytes or whole body, but not altered when S6K1 was disrupted only in neurons or liver. Taken together, these data indicate that decreased S6K1 activity in liver is sufficient to delay the neurological and survival defects caused by deficiency of Complex I and suggest that mTOR signaling can modulate mitochondrial disease and metabolism via cell non-autonomous mechanisms.

The inactivation of ribosomal protein S6 kinase 1 (S6K1) recapitulates aspects of caloric restriction and mTORC1 inhibition to achieve prolonged longevity in invertebrate and mouse models. In addition to delaying normative aging, inhibition of mTORC1 extends the shortened lifespan of yeast, fly, and mouse models with severe mitochondrial disease. Here we tested whether disruption of S6K1 can recapitulate the beneficial effects of mTORC1 inhibition in the Ndufs4 knockout (NKO) mouse model of Leigh Syndrome caused by Complex I deficiency. These NKO mice develop profound neurodegeneration resulting in brain lesions and death around 50-60 days of age. Our results show that liver-specific, as well as whole body, S6K1 deletion modestly prolongs survival and delays onset of neurological symptoms in NKO mice. In contrast, we observed no survival benefit in NKO mice specifically disrupted for S6K1 in neurons or adipocytes. Body weight was reduced in WT mice upon disruption of S6K1 in adipocytes or whole body, but not altered when S6K1 was disrupted only in neurons or liver. Taken together, these data indicate that decreased S6K1 activity in liver is sufficient to delay the neurological and survival defects caused by deficiency of Complex I and suggest that mTOR signaling can modulate mitochondrial disease and metabolism via cell non-autonomous mechanisms.

The inactivation of ribosomal protein S6 kinase 1 (S6K1) recapitulates aspects of caloric restriction and mTORC1 inhibition to achieve prolonged longevity in invertebrate and mouse models. In addition to delaying normative aging, inhibition of mTORC1 extends the shortened lifespan of yeast, fly, and mouse models with severe mitochondrial disease. Here we tested whether disruption of S6K1 can recapitulate the beneficial effects of mTORC1 inhibition in the Ndufs4 knockout (NKO) mouse model of Leigh Syndrome caused by Complex I deficiency. These NKO mice develop profound neurodegeneration resulting in brain lesions and death around 50-60 days of age. Our results show that liver-specific, as well as whole body, S6K1 deletion modestly prolongs survival and delays onset of neurological symptoms in NKO mice. In contrast, we observed no survival benefit in NKO mice specifically disrupted for S6K1 in neurons or adipocytes. Body weight was reduced in WT mice upon disruption of S6K1 in adipocytes or whole body, but not altered when S6K1 was disrupted only in neurons or liver. Taken together, these data indicate that decreased S6K1 activity in liver is sufficient to delay the neurological and survival defects caused by deficiency of Complex I and suggest that mTOR signaling can modulate mitochondrial disease and metabolism via cell non-autonomous mechanisms.

The inactivation of ribosomal protein S6 kinase 1 (S6K1) recapitulates aspects of caloric restriction and mTORC1 inhibition to achieve prolonged longevity in invertebrate and mouse models. In addition to delaying normative aging, inhibition of mTORC1 extends the shortened lifespan of yeast, fly, and mouse models with severe mitochondrial disease. Here we tested whether disruption of S6K1 can recapitulate the beneficial effects of mTORC1 inhibition in the Ndufs4 knockout (NKO) mouse model of Leigh Syndrome caused by Complex I deficiency. These NKO mice develop profound neurodegeneration resulting in brain lesions and death around 50-60 days of age. Our results show that liver-specific, as well as whole body, S6K1 deletion modestly prolongs survival and delays onset of neurological symptoms in NKO mice. In contrast, we observed no survival benefit in NKO mice specifically disrupted for S6K1 in neurons or adipocytes. Body weight was reduced in WT mice upon disruption of S6K1 in adipocytes or whole body, but not altered when S6K1 was disrupted only in neurons or liver. Taken together, these data indicate that decreased S6K1 activity in liver is sufficient to delay the neurological and survival defects caused by deficiency of Complex I and suggest that mTOR signaling can modulate mitochondrial disease and metabolism via cell non-autonomous mechanisms.

The inactivation of ribosomal protein S6 kinase 1 (S6K1) recapitulates aspects of caloric restriction and mTORC1 inhibition to achieve prolonged longevity in invertebrate and mouse models. In addition to delaying normative aging, inhibition of mTORC1 extends the shortened lifespan of yeast, fly, and mouse models with severe mitochondrial disease. Here we tested whether disruption of S6K1 can recapitulate the beneficial effects of mTORC1 inhibition in the Ndufs4 knockout (NKO) mouse model of Leigh Syndrome caused by Complex I deficiency. These NKO mice develop profound neurodegeneration resulting in brain lesions and death around 50-60 days of age. Our results show that liver-specific, as well as whole body, S6K1 deletion modestly prolongs survival and delays onset of neurological symptoms in NKO mice. In contrast, we observed no survival benefit in NKO mice specifically disrupted for S6K1 in neurons or adipocytes. Body weight was reduced in WT mice upon disruption of S6K1 in adipocytes or whole body, but not altered when S6K1 was disrupted only in neurons or liver. Taken together, these data indicate that decreased S6K1 activity in liver is sufficient to delay the neurological and survival defects caused by deficiency of Complex I and suggest that mTOR signaling can modulate mitochondrial disease and metabolism via cell non-autonomous mechanisms.

El salario sería una renta del trabajo, el coche de empresa también si lo usas con fines personales, al igual que el alquiler de la casa que te paga la empresa, la pensión pública de jubilación o determinadas becas y ayudas estatales, por ejemplo.

Alpha-fetoprotein (AFP) is a major serum protein produced during fetal development. Experimental findings suggest that AFP has antiestrotrophic activity and that it can be developed as a therapeutic agent to treat existing estrogen-dependent breast cancer or to prevent premalignant foci from developing into breast cancer. The antiestrotrophic activity of AFP was reported to be localized to a peptide consisting of amino acids 447^480, a 34-mer peptide termed P447. A series of parsings and substitutions of amino acids in the P447 sequence was intended to identify the shortest analog which retained antiestrotrophic activity. Peptides related to P447 were generated using solid phase peptide synthesis. Several shorter peptides, including an 8-mer called P472-2 (amino acids 472^479, peptide sequence EMTPVNPG), retained activity, whereas peptides shorter than eight amino acid residues were inactive. The dose-related antiestrotrophic activity of AFP-derived peptides was determined in an immature mouse uterine growth assay that measures their ability to inhibit estradiolstimulated uterine growth. In this assay, the maximal inhibitory activities exhibited by peptide P472-2 (49%), by peptide P447 (45%), and by intact AFP (35^45%) were comparable. The octapeptide P472-2 was also active against estradiol-stimulated growth of T47D human breast cancer cells in culture. These data suggest that peptide P472-2 is the minimal sequence in AFP, which retains the antiestrotrophic activity found with the full-length molecule. The synthetic nature and defined structure of this 8-mer peptide suggest that it can be developed into a new drug which opposes the action of estrogen, perhaps including the promotional effects of estradiol in the development of human breast cancer.

The dispersion properties of structured metamaterials consisting of strips of a copper wire (electron subsystem) and square copper split-ring resonators (magnetic subsystem) with different and coinciding resonant frequencies are studied. In a narrow frequency band above the resonant frequency of the electron subsystem, the structured metamaterial is described by a negative refractive index. In addition to this, there are some peculiar properties observed in these metamaterials. Among these properties is the nonanalytic behavior of the real part of the refractive index as a function of the frequency with a discontinuity of its derivative in the metamaterial with two resonances. It is also shown that the superluminal, slow, and backward microwaves can exist in the structured metamaterials. However, in the absence of gain components, only the slow microwaves can propagate considerably.