Role of selenium depletion in the effects of dialysis on mood and behavior

Depression and behavioral problems are common in patients undergoing dialysis. Researchers have reported that serum selenium concentrations are generally lower in dialysis patients than in healthy controls. Considerable evidence suggests that selenium deprivation leads to depressed mood, and high dietary or supplementary selenium seems to improve mood. Low plasma selenium concentrations in the elderly are significantly associated with senility and cognitive decline. The author suggests that dialysis-related selenium loss may play a role in biological mechanisms of psychiatric disorders in dialysis patients.     

Etiopathogenesis of depression in patients with alcoholism: role of changes in thyroid function

Alcoholism poses a significant risk for the development of depression. Alcohol abuse and dependence significantly affect thyroid function. Considerable evidence suggests that minor changes in thyroid function may affect mood and behavior. The author suggests that alcohol-induced changes in thyroid function may contribute the development of depression in patients with alcoholism. Probably, alcohol-induced alterations in thyroid function are not a sufficient cause of depression. Most likely, they work in concert with inherited, acquired, and environmental risk factors. Alcohol may be particularly damaging to the impaired thyroid gland. Studies of the interrelationships between alcoholism and depression may help elucidate the causes of both.     

parkin mutation analysis in clinic patients with early-onset Parkinson [corrected] disease

parkin Mutations are the most common identified cause of Parkinson's disease (PD). It has been suggested that patients with young-onset PD be screened for parkin mutations as a part of their clinical work-up. The aim of this study was to assess parkin mutation frequency in a clinical setting, correlate genotype with phenotype, and evaluate the current justification for clinical parkin testing. Patients were selected from a movement disorder clinic based on diagnosis of PD and onset age 相似文献   

Role of moxifloxacin for the treatment of community-acquired [corrected] complicated intra-abdominal infections in Taiwan

Complicated intra-abdominal infections (cIAIs) are common yet serious infections that can potentially lead to substantial morbidity and morbidity. As an essential adjunct to source control, the goals of antimicrobial therapy are to promote patient recovery, reduce recurrence risk, and prevent antimicrobial resistance. The current international guidelines on the empirical treatment of community-acquired complicated IAIs were published by the Infectious Diseases Society of America (IDSA) and Surgical Infections Society (SIS) in 2010. These guidelines all recommend the use of a fluoroquinolone (ciprofloxacin or levofloxacin) plus metronidazole for mild-to-moderate- and high-severity cases. Moxifloxacin monotherapy is recommended by the current IDSA/SIS guidelines for the treatment of mild-to-moderate complicated IAIs. Moxifloxacin has demonstrated a broad spectrum coverage of both aerobic and anaerobic pathogens, good tissue penetration into the gastrointestinal tract, and a good tolerability profile. Clinical data have demonstrated that moxifloxacin is at least as effective as other standard therapeutic regimens recommended by current clinical guidelines. Due to the high rates of extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae and fluoroquinolone-resistant Enterobacteriaceae among isolates causing community-acquired IAIs in Asia, any fluoroquinolones (including moxifloxacin) are not recommended as drugs of choice for the empirical treatment of community-acquired IAIs, particularly in countries (China, India, Thailand, and Vietnam) with fluoroquinolone resistance rates among Escherichia coli isolates of >20%. Given the low rates of fluoroquinolone-resistant (<20%) and extended-spectrum β-lactamase (ESBL)-producing (<10%) Enterobacteriaceae isolates associated community-acquired IAIs in Taiwan, it appears that moxifloxacin is considered an appropriate first-line therapy for patients with community-acquired complicated IAIs in this country.     

Plasma NPY concentrations during tryptophan and sham depletion in medication-free patients with remitted depression

BACKGROUND: Neuropeptide Y (NPY) and serotonergic systems have been implicated in the pathophysiology of depression but have not yet been linked together. METHODS: In a randomized, double-blind crossover study, 28 medication-free patients with remitted depression and 26 healthy control subjects underwent tryptophan depletion (TD) and sham depletion. Plasma NPY concentrations were determined at baseline and at +5, +7, and +24 h during TD and sham depletion, respectively. Hamilton Depression Rating Scale (HDRS, 24-item) scores were assessed at baseline and at +7 and +24 h after TD and sham depletion, respectively. RESULTS: There was no difference between healthy subjects and patients with remitted depression in baseline plasma NPY concentrations and in plasma NPY concentrations during TD and sham depletion, respectively. Plasma NPY concentrations did not differ between TD and sham depletion. At no time point there was an association between HDRS scores and plasma NPY concentrations in patients with remitted depression. LIMITATIONS: Plasma NPY concentrations in rMDD patients were not obtained during the symptomatic phase of the illness. Only peripheral measurements of NPY were used. CONCLUSIONS: Decreased plasma NPY concentrations, as described previously during a spontaneous episode of major depression, appear as state but not as trait marker in depression. No evidence was found for an involvement of plasma NPY in relapse during TD. There appears no direct functional link between serotonergic neurotransmission and plasma NPY concentrations.     

Role of peroxynitrite-modified biomolecules in the etiopathogenesis of systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease characterized by autoantibodies directed against various biomolecules. The initial immunogens that drive the development of SLE are unknown, but characteristics of the immune response in SLE suggest that it is an antigen-driven response, and a chromatin antigen could be one of the immunogens for the production of antinuclear antibodies (ANA) in SLE. Other factors implicated in the pathogenesis of SLE include nitrogen-free radicals such as nitric oxide and peroxynitrite. The free radical-mediated damage to proteins results in the modification of amino acid residues, cross-linking of side chains and fragmentation. The tyrosine residues in proteins are susceptible to attack by various reactive nitrogen intermediates, including peroxynitrite to form 3-nitrotyrosine (3-NT). The presence of nitrated proteins in vivo indicates that peptides derived from the proteolytic degradation of modified proteins could serve as neoantigens. Histones are highly conserved proteins that are rich in basic amino acids lysine and arginine. Autoantibodies against histones and anti-DNA antibodies are present in SLE. The anti-DNA autoantibodies coexist with anti-histone autoantibodies and may react with chromatin-associated histones and histone complexes. Elevated levels of reactive nitrogen species (RNS) in SLE patients suggest a possible role in the pathogenesis of the disease. The alteration of proteins resulting from photomodification or peroxynitrite could lead to the development of antibodies. Therefore, the modified proteins or photoadducts could have important implications in autoimmunity, and understanding the pathophysiology of peroxynitrite-modified biomolecules could lead to a better understanding of autoimmune phenomenon in SLE.     

Frequent [corrected] hyperphosphorylation of ribosomal protein S6 [corrected] in lymphangioleiomyomatosis-associated angiomyolipomas.

Lymphangioleiomyomatosis is a progressive lung disease characterized by a diffuse proliferation of pulmonary smooth muscle cells and cystic degeneration. Lymphangioleiomyomatosis can occur either independently of other disease or in association with tuberous sclerosis complex, a tumor-suppressor gene syndrome caused by mutations that inactivate either TSC1 or TSC2. TSC2 mutations and loss of heterozygosity have been identified in sporadic lymphangioleiomyomatosis-associated angiomyolipomas, thus implicating the TSC/Ras homolog-enriched in brain (Rheb)/mammalian target of Rapamycin (mTOR)/p70 S6 kinase signaling pathway in their pathogenesis. This study was undertaken to determine whether the mTOR/p70 S6 kinase signaling pathway is activated in lymphangioleiomyomatosis-associated angiomyolipomas lacking TSC1/TSC2 loss of heterozygosity. Phospho-ribosomal protein S6 (Ser235/236) immunohistochemistry was performed on five lymphangioleiomyomatosis-associated angiomyolipomas, two matched lymphangioleiomyomatosis pulmonary samples, and three sporadic angiomyolipomas. TSC1/TSC2 loss of heterozygosity was previously excluded in these angiomyolipomas. Moderate or strong phospho-ribosomal protein S6 immunoreactivity was found in all lymphangioleiomyomatosis-associated and sporadic angiomyolipomas, suggesting a high incidence of mTOR/p70 S6 kinase signaling pathway activation despite a lack of TSC1/TSC2 loss of heterozygosity. Focally positive phospho-S6 staining was also evident in both lymphangioleiomyomatosis pulmonary samples. We hypothesized that this S6 hyperphosphorylation could reflect mutational activation of Rheb or Rheb-like protein (RhebL1), Ras family members which directly activate mTOR. Mutational analysis performed on DNA from these eight angiomyolipomas plus five additional sporadic angiomyolipomas did not reveal mutations in exons 3 and 4 (homologous sites of Ras activating mutations) of either Rheb or RhebL1. These data suggest that activation of the Rheb/mTOR/p70 S6 kinase pathway is related to the pathogenesis of lymphangioleiomyomatosis-associated and sporadic angiomyolipomas lacking TSC1/TSC2 loss of heterozygosity. This high incidence of mTOR signaling pathway activation suggests that treatment with mTOR inhibitors, such as Rapamycin, may benefit patients with angiomyolipomas independent of the detection of TSC1/TSC2 loss of heterozygosity.     

The influence of alcoholism on the course of depression

The clinical course of 289 patients with primary non-bipolar major depression without concurrent alcoholism was compared with that of 79 patients with non-bipolar major depression with concurrent alcoholism. Neither patient group suffered from dysthymia or current drug abuse. Contrary to expectations, the two groups did not differ on time to recovery from the major depression, time to relapse into a subsequent major depression, or various cross-sectional clinical ratings at 2 years. The two groups did differ on psychosocial status. Although they were equally impaired at index, the alcoholism group maintained significantly lower levels of psychosocial functioning throughout the 2-year follow-up period. Interpersonal relation with spouse was particularly worse among the alcoholic group.     

Periacinar collagenization in patients with chronic alcoholism

To examine the development of pancreatic fibrosis In alcoholics, the fibrosis types grouped according to Martin's classification were examined by immunohlstochemistty using an antibody against α-smooth muscle actin (α-SMA). The initial stage of periacinar collagenizatlon was also Investigated by electron microscopy. The total incidence of pancreatlc fibrosis at autopsy of the 29 alcoholics was significantly higher than that of the 40 non-alcoholics. lntralobular sclerosis was observed to be the most frequent type of fibrosls regardless of alcohol intake. No differences in the enhancement of α-SMA expresslon in each type of fibrosis were found between the alcoholics and non-alcoholics. Electron microscopically, myofibroblasts were found around acini in the early stage of periacinar collagenization, and were accompanled by numerous fine filaments (8–15 nm in diameter). The various changes In zymogen granules (ZG), lysosomes and lipld droplets were augmented in the acinar cells of alcoholics. Medlumdensity materials were also found in dilated rough endoplasmic retlculum (RER). The contents of ZG and RER occasionally leaked out. In conclusion, pancreatlc fibrosis was increased in alcoholics; myofibroblasts may play an important role in the initial stage of periacinar collagenizatlon; and the intracellular transport blockage of protein as represented by abnormalities of ZG, ER and lysosomes may contribute to the development of periacinar collagenization.     

Structural alterations of the brain in patients with chronic alcoholism

The brain was studied in 14 healthy persons and in 23 patients with symptoms of alcoholism. Sclerosis and hyalinosis of the vessels and dystrophic, atrophic and hypertrophic neurocyte changes were found in the brain of patients as well as calcium petrificates, cysts, foci of demyelinisation and diffuse microgliosis of cerebral tissue. The share of neural cells was less due to their atrophy and death while glial component share was increased.     

Effects of selenium depletion and selenium repletion by choice feeding on selenium status of young and old laying hens

We investigated the effect of choice feeding two diets with different selenium (Se) content to young and old moderately Se-deficient laying hens on serum Se (SSe), glutathione peroxidase (GPX), vitamin E, creatine kinase (CK), aspartate aminotransferase (ASAT), thyroxine (T4) and triiodothyronine (T3). Each of two consecutive study parts (I and II) with the same hens and treatments began with a 6-week baseline period (Medium-Se diet), followed by a 9-week depletion period (Low-Se or Medium-Se diet), followed by a 6-week choice period with two different diets offered simultaneously (Medium-Se/Low-Se, Medium-Se/High-Se, or Low-Se/High-Se). During both depletion periods, SSe and GPX gradually decreased, whereas T4 gradually increased in hens fed Low-Se confirming gradual Se-depletion. T3 decreased transiently in young hens only. As reported earlier, Se-deficient hens preferred High-Se over Low-Se diet during the first 3 weeks of choice feeding in part I, not however in part II. This preference resulted in higher SSe in these hens. GPX activity did not reflect feed preference, probably because Se-intake exceeded Se-requirement for maximal GPX activity. In Part II, hens depleted with Low-Se diet had higher SSe when previously offered High-Se diet in either combination, than when offered Low-Se/Medium-Se, presumably due to Se-stores built during choice feeding in part I, which possibly prevented development of Se-deficiency in part II. In addition, in older hens, Se depletion proceeded faster, whereas Se-repletion by choice feeding was slower than in young hens, indicating the increase in Se requirement with advancing age. Vitamin E, ASAT and CK remained largely unchanged by the treatments.     

Lymphocyte depletion in patients with rheumatoid arthritis

Sixteen patients with severe rheumatoid arthritis, marked inflammation of the synonvial membrane and high rheumatoid titer were cannulated by the thoracic duct for a period ranging between 82 up to 100 days. The patients being not under any medication during that time. Quantitative and qualitative analysis of the lymphocytes were performed, as well as responses to mitogens, rheumatoid factor, circulating antibodies and delayed hypersensitivity. By the 14th day nearly all the patients had a partial or almost complete remission of their disease. No complications were observed. These results will be discussed.     

Neurocognitive dysfunction in patients diagnosed with schizophrenia and alcoholism

The authors administered the Halstead-Reitan Neuropsychological Test Battery to schizophrenic groups with (n = 54) and without (n = 217) coexisting alcoholism, nonschizophrenic groups with alcoholism (n = 231), and a patient comparison group (n = 145) to determine the extent of additive cognitive impairment in schizophrenia associated with alcoholism and to compare cognitive function in alcoholism and schizophrenia. The additive effects of alcoholism on cognitive dysfunction in schizophrenia were subtle but were consistently identifiable. Cognitive dysfunction in alcoholism was less severe than in schizophrenia with or without alcoholism. The magnitude of additive effects of alcoholism on cognitive dysfunction in schizophrenia was age related with a significant interaction between age and presence or absence of alcoholism on a global index of cognitive dysfunction.