Miracle-dz/UniFAR-FTUs huggingface dataset:
Locustatachykinin immunoreactivity in the blowfly central nervous system and intestine

An antiserum raised against locustatachykinin I, one of four myotropic peptides that have been isolated from the locust brain and corpora cardiaca, was characterized by enzyme‐linked immunosorbent assay (ELISA) and used for immunocytochemical detection of neurons and endocrine cells in the nervous system and intestine of the blowfly Calliphora vomitoria. The ELISA characterization indicated that the antiserum recognizes the common C‐terminus sequence of the locustatachykinins I‐III. Hence, the cross reaction with locustatachykinin IV is less, and in competitive ELISAs no cross reaction was detected with a series of vertebrate tachykinins tested. It was also shown that the antiserum recognized material in extracts of blowfly heads, as measured in ELISA. In high‐performance liquid chromatography the extracted locustatachykinin‐like immunoreactive (Lom TK‐LI) material eluted in two different ranges. A fairly large number of LomTK‐LI neurons was detected in the blowfly brain and thoracicoabdominal ganglion. A total of about 160 LomTK‐LI neurons was seen in the proto‐, deuto‐, and tritocerebrum and subesophageal ganglion. Immunoreactive processes from these neurons could be traced in many neuropil regions of the brain: superior and dorsomedian protocerebrum, optic tubercle, fan‐shaped body and ventral bodies of the central complex, all the glomeruli of the antennal lobes, and tritocerebral and subesophageal neuropil. No immunoreactivity was seen in the mushroom bodies or the optic lobes. In the fused thoracicoabdominal ganglion, 46 LomTK‐LI neurons could be resolved. The less evolved larval nervous system was also investigated to obtain additional information on the morphology and projections of immunoreactive neurons. In neither the larval nor the adult nervous systems could we identify any efferent or afferent immunoreactive axons or neurosecretory cells. The widespread distribution of LomTK‐LI material in interneurons suggests an important role of the native peptide(s) as a neurotransmitter or neuromodulator within the central nervous system. Additionally a regulatory function in the intestine is indicated by the presence of immunoreactivity in endocrine cells of the midgut.
Transient Covalent Interactions of Newly Synthesized Thyroglobulin with Oxidoreductases of the Endoplasmic Reticulum*

Background: Secretory proteins acquire their native three-dimensional conformation through repeated brief interactions with ER chaperones and oxidoreductases. Results: We have captured and defined previously unidentified disulfide adducts of newly synthesized thyroglobulin with ERp72 and CaBP1/P5. Conclusion: Multiple oxidoreductases simultaneously engage thyroglobulin during its early folding in the ER. Significance: Distinct chaperone/oxidoreductase partners coordinately engage this multi-domain secretory protein to promote its advancement to the native state. Newly synthesized thyroglobulin (Tg), the thyroid prohormone, forms detectable high molecular weight mixed disulfide adducts: until now, only Tg “adduct B” was identified as primarily engaging the endoplasmic reticulum oxidoreductases ERp57 and protein disulfide isomerase. Here, we demonstrate that the faster migrating Tg adduct C primarily engages the CaBP1/P5 oxidoreductase, whereas the slower migrating Tg adduct A primarily engages ERp72. Upon siRNA-mediated knockdown of CaBP1/P5 or ERp72, adducts C or A, respectively, are decreased. Within the three Tg adduct bands that do not exhibit a precursor-product relationship, Tg exhibits distinct oxidation patterns. We present evidence suggesting that disulfide maturation occurs within Tg monomers engaged in each of the adduct bands. Moreover, the same Tg substrate molecules can form simultaneous mixed disulfides with both CaBP1/P5 and protein disulfide isomerase, although these are generally viewed as components of distinct oxidoreductase-chaperone protein complexes. Such substrate-oxidoreductase combinations offer Tg the potential for simultaneous oxidative maturation along different parallel tracks leading to the native state.
Oxygen regulates tissue nitrite metabolism.

AIMS Once dismissed as an inert byproduct of nitric oxide (NO) auto-oxidation, nitrite (NO(2)(-)) is now accepted as an endocrine reservoir of NO that elicits biological responses in major organs. While it is known that tissue nitrite is derived from NO oxidation and the diet, little is known about how nitrite is metabolized by tissue, particularly at intermediate oxygen tensions. We investigated the rates and mechanisms of tissue nitrite metabolism over a range of oxygen concentrations. RESULTS We show that the rate of nitrite consumption differs in each organ. Further, oxygen regulates the rate and products of nitrite metabolism. In anoxia, nitrite is reduced to NO, with significant formation of iron-nitrosyl proteins and S-nitrosothiols. This hypoxic nitrite metabolism is mediated by different nitrite reductases in each tissue. In contrast, low concentrations (∼3.5 μM) of oxygen increase the rate of nitrite consumption by shifting nitrite metabolism to oxidative pathways, yielding nitrate. While cytochrome P(450) and myoglobin contribute in the liver and heart, respectively, mitochondrial cytochrome c oxidase plays a significant role in nitrite oxidation, which is inhibited by cyanide. Using cyanide to prevent artifactual nitrite decay, we measure metabolism of oral and intraperitoneally administered nitrite in mice. INNOVATION These data provide insight into the fate of nitrite in tissue, the enzymes involved in nitrite metabolism, and the role of oxygen in regulating these processes. CONCLUSION We demonstrate that even at low concentrations, oxygen is a potent regulator of the rate and products of tissue nitrite metabolism.
Explaining Emergence and Consequences of Specific Formal Controls in IS Outsourcing -- A Process-View

IS outsourcing projects often fail to achieve project goals. To inhibit this failure, managers need to design formal controls that are tailored to the specific contextual demands. However, the dynamic and uncertain nature of IS outsourcing projects makes the design of such specific formal controls at the outset of a project challenging. Hence, the process of translating high-level project goals into specific formal controls becomes crucial for success or failure of IS outsourcing projects. Based on a comparative case study of four IS outsourcing projects, our study enhances current understanding of such translation processes and their consequences by developing a process model that explains the success or failure to achieve high-level project goals as an outcome of two unique translation patterns. This novel process-based explanation for how and why IS outsourcing projects succeed or fail has important implications for control theory and IS project escalation literature.
Neural correlates of antinociception in borderline personality disorder.

CONTEXT A characteristic feature of borderline personality disorder (BPD) is self-injurious behavior in conjunction with stress-induced reduction of pain perception. Reduced pain sensitivity has been experimentally confirmed in patients with BPD, but the neural correlates of antinociceptive mechanisms in BPD are unknown. We predicted that heat stimuli in patients with BPD would activate brain areas concerned with cognitive and emotional evaluation of pain. OBJECTIVE To assess the psychophysical properties and neural correlates of altered pain processing in patients with BPD. DESIGN Case-control study. SETTING A university hospital. PARTICIPANTS Twelve women with BPD and self-injurious behavior and 12 age-matched control subjects. INTERVENTIONS Psychophysical assessment and blood oxygen level-dependent functional magnetic resonance imaging during heat stimulation with fixed-temperature heat stimuli and individual-temperature stimuli adjusted for equal subjective pain in all the participants. MAIN OUTCOME MEASURE Blood oxygen level-dependent functional magnetic resonance imaging signal changes during heat pain stimulation. RESULTS Patients with BPD had higher pain thresholds and smaller overall volumes of activity than controls in response to identical heat stimuli. When the stimulus temperature was individually adjusted for equal subjective pain level, overall volumes of activity were similar, although regional patterns differed significantly. Patient response was greater in the dorsolateral prefrontal cortex and smaller in the posterior parietal cortex. Pain also produced neural deactivation in the perigenual anterior cingulate gyrus and the amygdala in patients with BPD. CONCLUSION The interaction between increased pain-induced response in the dorsolateral prefrontal cortex and deactivation in the anterior cingulate and the amygdala is associated with an antinociceptive mechanism in patients with BPD.
Intermediate-term follow-up after ankle distraction for treatment of end-stage osteoarthritis.

BACKGROUND Treatment of end-stage ankle osteoarthritis remains challenging, especially in young patients. Initial reports have shown early benefits of joint distraction for the treatment of ankle osteoarthritis. We report the five to ten-year results of a previously described patient cohort following ankle distraction surgery. METHODS All thirty-six patients who had undergone ankle distraction surgery between December 2002 and October 2006 were contacted. Patients were evaluated by a clinical investigator and completed the Ankle Osteoarthritis Scale (AOS) and Short Form-36 (SF-36) surveys. Radiographs as well as computed tomography and magnetic resonance imaging scans of the ankles were obtained at the follow-up visits. RESULTS Twenty-nine patients (81%) were followed for a minimum of five years (mean and standard deviation, 8.3 ± 2.2 years). Sixteen (55%) of the twenty-nine patients still had the native ankle joint whereas thirteen patients (45%) had undergone either ankle arthrodesis or total ankle arthroplasty. Positive predictors of ankle survival included a better AOS score at two years (hazard ratio [HR] = 0.048, 95% confidence interval [CI] = 0.0028 to 0.84, p = 0.04), older age at surgery (HR = 0.91, 95% CI = 0.83 to 0.99, p = 0.04), and fixed distraction (HR = 0.094, 95% CI = 0.017 to 0.525, p < 0.01). Radiographs and advanced imaging revealed progression of ankle osteoarthritis at the time of final follow-up. CONCLUSIONS Ankle function following joint distraction declines over time. Patients should be well informed of the commitment that they must make during the treatment period as well as the long-term results after surgery.
Primate cytomegalovirus assembly protein: genome location and nucleotide sequence

A cDNA encoding the 37-kilodalton (kDa) capsid assembly protein of cytomegalovirus (CMV) strain Colburn was isolated from a lambda gt11 library constructed from CMV Colburn-infected human fibroblast RNA. RNA transcribed in vitro from this cDNA was translated in vitro to give a 40-kDa protein whose electrophoretic mobility during sodium dodecyl sulfate-polyacrylamide gel electrophoresis and fragmentation pattern following partial proteolysis were indistinguishable from those of authentic assembly protein precursor. The position of the assembly protein gene was mapped to the EcoRI F, XbaI R, and SalI U restriction fragments, near the middle of the CMV Colburn genome, by Southern hybridizations using the cloned assembly protein cDNA as a probe. Similar sequences were identified by cross-hybridizations in colinear regions of the genomes of human CMV strains Towne and AD169: specifically, in the HindIII H, BamHI V, and EcoRI A fragments of Towne and in the HindIII L and BglII S fragments of AD169. The predominant transcript of the assembly protein gene was determined to be approximately 1 kilobase in size; however, a larger transcript (1.8 kilobases) was also identified. The nucleotide sequence of the assembly protein cDNA was determined and found to contain a single long open reading frame predicted to encode a polypeptide of 36.6 to 37 kDa, close to the 40-kDa size determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis for the assembly protein precursor. The presence of a single cysteine residue at the carboxy-terminal end of this open reading frame is consistent with data from biochemical studies and indicates that processing of the assembly protein precursor includes a proteolytic cleavage that removes its carboxyl end.
Why do people die in famines? Evidence from three island populations.

There is surprisingly little consensus about what people die of during famines. In this paper, the causes of the increases in mortality during the Greek famine of 1941–43 are examined. The focus of the study is three island populations: Syros, Hios, and Mykonos. Death registration for these islands was not disrupted during the famine and the records give cause of death, certified by a doctor. Archival material and hospital records are utilized to assess public health during the famine. The findings point to the overwhelming importance of starvation for increased mortality during the famine and the virtual absence of either significant epidemics of infectious diseases or a breakdown in the public health system. The paper concludes by comparing the findings for the Greek famine with those for other famines. A model that attempts to explain the different courses that famine mortality can take is proposed.
Glutamate‐induced activation of nitric oxide synthase is impaired in cerebral cortex in vivo in rats with chronic liver failure

It has been proposed that impairment of the glutamate‐nitric oxide‐cyclic guanosine monophosphate (cGMP) pathway in brain contributes to cognitive impairment in hepatic encephalopathy. The aims of this work were to assess whether the function of this pathway and of nitric oxide synthase (NOS) are altered in cerebral cortex in vivo in rats with chronic liver failure due to portacaval shunt (PCS) and whether these alterations are due to hyperammonemia. The glutamate‐nitric oxide‐cGMP pathway function and NOS activation by NMDA was analysed by in vivo microdialysis in cerebral cortex of PCS and control rats and in rats with hyperammonemia without liver failure. Similar studies were done in cortical slices from these rats and in cultured cortical neurons exposed to ammonia. Basal NOS activity, nitrites and cGMP are increased in cortex of rats with hyperammonemia or liver failure. These increases seem due to increased inducible nitric oxide synthase expression. NOS activation by NMDA is impaired in cerebral cortex in both animal models and in neurons exposed to ammonia. Chronic liver failure increases basal NOS activity, nitric oxide and cGMP but reduces activation of NOS induced by NMDA receptors activation. Hyperammonemia is responsible for both effects which will lead, independently, to alterations contributing to neurological alterations in hepatic encephalopathy.
Traumatic brain injury in the prodromal period of Parkinson's disease: A large epidemiological study using medicare data

Studies suggest a greater risk of Parkinson's disease (PD) after traumatic brain injury (TBI), but it is possible that the risk of TBI is greater in the prodromal period of PD. We aimed to examine the time‐to‐TBI in PD patients in their prodromal period compared to population‐based controls.
Screening for Hematological Disorders in Mosaic Down Syndrome

Children with Down syndrome (DS) have increased risk for multiple medical conditions with published health care guidelines. Current guidelines do not specify whether or not they apply to mosaic DS (mDS). We surveyed families of patients with mDS regarding screening, including monitoring practices as well as complications identified. Hematological complications were similar to those reported in nonmosaic DS. Of 91 parents of children with mDS surveyed, only 69% had ever had a screening lab; only 57% had ever had a screening complete blood count (CBC). Younger children were less likely to be screened (for CBC, 50% of 0- to 3-year-olds vs 90% of 4- to 12-year-olds; P = 0.0036). Screening practices are suboptimal, with the youngest children at greatest risk. Comparing reported screening practices with physician adherence, there was discrepancy between perceptions of adherence and perceptions of practice. Children with mDS should be monitored on the same schedule as other children with DS.
Cardiac actin is the major actin gene product in skeletal muscle cell differentiation in vitro

We examined the expression of alpha-skeletal, alpha-cardiac, and beta- and gamma-cytoskeletal actin genes in a mouse skeletal muscle cell line (C2C12) during differentiation in vitro. Using isotype-specific cDNA probes, we showed that the alpha-skeletal actin mRNA pool reached only 15% of the level reached in adult skeletal muscle and required several days to attain this peak, which was then stably maintained. However, these cells accumulated a pool of alpha-cardiac actin six times higher than the alpha-skeletal actin mRNA peak within 24 h of the initiation of differentiation. After cells had been cultured for an additional 3 days, this pool declined to 10% of its peak level. In contrast, over 95% of the actin mRNA in adult skeletal muscle coded for alpha-actin. This suggests that C2C12 cells express a pattern of sarcomeric actin genes typical of either muscle development or regeneration and distinct from that seen in mature, adult tissue. Concurrently in the course of differentiation the beta- and gamma-cytoskeletal actin mRNA pools decreased to less than 10% of their levels in proliferating cells. The decreases in beta- and gamma-cytoskeletal actin mRNAs are apparently not coordinately regulated.
A Comparative Study of Tissue Inhibitor of Metalloproteinases-1 Levels in Plasma and Tumour Tissue from Patients with Primary Breast Cancer and in Plasma from Patients with Metastatic Breast Cancer

Objective: Tissue inhibitor of metalloproteinases-1 (TIMP-1) has been investigated as a potential tumour marker in breast cancer. Here we investigated the correlation between TIMP-1 in tumour tissue and plasma to evaluate whether TIMP-1 in plasma is actually a surrogate marker for TIMP-1 in primary tumours. Furthermore, we assessed whether increased TIMP-1 levels in plasma could be indicative of tumour progression in patients with advanced breast cancer. Methods: Tumour tissue and preoperatively collected plasma samples from 96 primary breast cancer patients were included together with plasma samples from 46 patients with advanced disease. TIMP-1 levels were measured by ELISA. Results: TIMP-1 levels in plasma (median 81.5 ng/ml, range 41.9–174.9) and tumour tissue (median 25.4 ng/mg of total protein, range 0–110.2) from primary breast cancer patients were not correlated (r = 0.05, p = 0.6). Plasma levels of TIMP-1 in primary breast cancer patients were significantly lower than levels in patients with advanced disease (median 108.7 ng/ml, range 59.7–560.7; p < 0.0001). Conclusions: Our findings suggest that TIMP-1 release into the blood might be controlled by an active mechanism. They also point to plasma TIMP-1 as a potential marker for predicting tumour progression and for monitoring tumour burden in metastatic breast cancer patients.
Micelle-vesicle transition in phospholipid-bile salt mixtures. A study by precision scanning calorimetry.

A systematic study of the micelle-vesicle transformation in phospholipid-bile salt mixtures using differential scanning calorimetry (DSC) indicates that the lipid undergoes a variety of changes in its thermal properties as mixed micellar solutions are diluted to concentrations at which vesicles form. In the experiments, micellar solutions of 50 mg/mL total lipid, containing sodium taurocholate (TC) and 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC), are diluted to concentrations corresponding to differing extents of aggregation of the TC with phospholipid. Turbidity and equilibrium dialysis measurements are used to establish boundaries between where micelles persist and where vesicles are formed and to determine the extent of aggregation of the TC with DPPC. At molar ratios Re of bound TC to DPPC greater than 0.3, micellar solutions are formed, while at Re less than 0.15 vesicles are evident upon dilution. As the transformation from micelles to vesicles occurs, the thermal transitions in the lipid change from broad, low Cp (max) peaks in the micelle region to multiple peaks of high cooperativity in regions of composition where lamellar structures and vesicles form. The DSC curves show that in the composition region corresponding to where bilayer micelles exist a new thermal phase forms, which has a melting transition near 32 degrees C, if the solutions are allowed to equilibrate for 48 h at 21 degrees C. Furthermore, at compositions between Re = 0 and 0.25, there is metastability in the lipid when equilibrated at 21 degrees C, but heating the lipid through the thermal transitions leads to reversible behavior. (ABSTRACT TRUNCATED AT 250 WORDS)
Qigong improves quality of life in women undergoing radiotherapy for breast cancer

Radiotherapy may lead to side effects that undermine patients' quality of life (QOL). Although mind‐body practices like qigong appear to improve QOL in cancer survivors, little is known about their benefits for patients who are receiving radiotherapy. Thus, in the current randomized controlled trial, the authors examined the efficacy of a qigong intervention on QOL in women with breast cancer during and after treatment.
Results of 136 curative hepatectomies with a safety margin of less than 10 mm for colorectal metastases

It is now established that liver resection is beneficial for metastases from colorectal cancer. Nevertheless, a surgical margin estimated at less than 10 mm at preoperative imaging is considered an absolute contraindication to surgery by some, and a relative contraindication by others. The true impact of the width of the margin on the prognosis is unclear.
Modified Chester Step Test in a Healthy Adult Population: Measurement Properties and Development of a Regression Equation to Estimate Test Duration.

OBJECTIVE Healthy working-aged adults performed the modified Chester Step Test (mCST) to (1) determine the effect of repetition on test duration, (2) report cardiorespiratory and symptom responses, (3) establish a regression equation to estimate duration, and (4) calculate the minimal detectable change (MDC) of the test. METHODS In this observational study conducted in a hospital physical therapy, adult participants aged 25 to 65 years who were healthy performed the mCST twice. This submaximal test required participants to step on and off a 20-cm step at a standardized cadence that increased every 2 minutes. The criteria for test completion was either the heart rate equal to 80% of age-predicted maximum or the onset of intolerable symptoms. The primary measure was time to test completion during the mCST (s). Cardiorespiratory and symptom responses were also collected during the mCST. RESULTS Eighty-three participants (40 men, mean [SD] age = 44 [12] y) completed data collection. There was no systematic effect of test repetition with median test duration of the first test (522 s, range = 400-631 s) and second test (501 s, range = 403-631 s). The test elicited moderate symptoms of breathlessness and leg fatigue. In the multivariable model, age, sex, weight, and height were retained as significant predictors of test duration (R2 = 0.48). The MDC was 119 s. CONCLUSION The mCST is a reliable and valid clinically applicable test of aerobic capacity in working aged adults. Independent pretest predictors can be used to estimate the clinical time required to complete the test. IMPACT The mCST was stable between test repetitions, suggesting no learning effect. For any given individual, a test duration change of two minutes represents change was beyond the natural variability. The mCST has good applicability to clinical settings.