Miracle-dz/UniFAR-FTUs huggingface dataset:
Formation and Stabilization of Rhizosheaths of Zea mays L. (Effect of Soil Water Content)

Field observations have shown that rhizosheaths of grasses formed under dry conditions are larger, more coherent, and more strongly bound to the roots than those formed in wet soils. We have quantified these effects in a model system in which corn (Zea mays L.) primary roots were grown through a 30-cm-deep prepared soil profile that consisted of a central, horizontal, “dry” (9% water content) or “wet” (20% water content) layer (4 cm thick) sandwiched between damp soil (15–17% water content). Rhizosheaths formed in dry layers were 5 times the volume of the subtending root. In wet layers, rhizosheaths were only 1.5 times the root volume. Fractions of the rhizosheath soil were removed from individual roots by three successive treatments; sonication, hot water, and abrasion. Sonication removed 50 and 90% of the soil from rhizosheaths formed in dry and wet soils, respectively. After the heat treatment, 35% of the soil still adhered to those root portions where rhizosheaths had developed in dry soil, compared with 2% where sheaths had formed in wet soil. Root hairs were 4.5 times more abundant and were more distorted on portions of roots from dry layers than from wet layers. Drier soil enhanced adhesiveness of rhizosheath mucilages and stimulated the formation of root hairs; both effects stabilize the rhizosheath. Extensive and stable rhizosheaths may function in nutrient acquisition in dry soils.
Bcl-2 and Bcl-xL Inhibit CD95-mediated Apoptosis by Preventing Mitochondrial Release of Smac/DIABLO and Subsequent Inactivation of X-linked Inhibitor-of-Apoptosis Protein*

Bcl-2 and Bcl-xL are reported to inhibit CD95-mediated apoptosis in “type II” but not in “type I” cells. In the present studies, we found that stimulation of CD95 receptors, with either agonistic antibody or CD95 ligand, resulted in the activation of caspase-8, which in turn processed caspase-3 between its large and small subunits. However, in contrast to control cells, those overexpressing either Bcl-2 or Bcl-xL displayed a distinctive pattern of caspase-3 processing. Indeed, the resulting p20/p12 caspase-3 was not active and did not undergo normal autocatalytic processing to form p17/p12 caspase-3, because it was bound to and inhibited by endogenous X-linked inhibitor-of-apoptosis protein (XIAP). Importantly, Bcl-2 and Bcl-xL inhibited the release of both cytochrome c and Smac from mitochondria. However, since Smac alone was sufficient to promote caspase-3 activityin vitro by inactivating XIAP, we proposed the existence of a death receptor-induced, Smac-dependent and apoptosome-independent pathway. This type II pathway was subsequently reconstituted in vitro using purified recombinant proteins at endogenous concentrations. Thus, mitochondria and associated Bcl-2 and Bcl-xL proteins may play a functional role in death receptor-induced apoptosis by modulating the release of Smac. Our data strongly suggest that the relative ratios of XIAP (and other inhibitor-of-apoptosis proteins) to active caspase-3 and Smac may dictate, in part, whether a cell exhibits a type I or type II phenotype.
Reply: Virological treatment failure of protease inhibitor therapy in an unselected cohort of HIV-infected patients.

Objective: To determine the rate of virological treatment failure with protease inhibitor therapy in unselected patients and to assess underlying risk factors. Design and setting: Retrospective study in two German tertiary care treatment centres. Patients: A total of 198 HIV-infected patients treated with protease inhibitors in 1996. Main outcome measures: Levels of HIV RNA 1-6 months after start of treatment; definition of treatment failure of < 1 log 10 reduction in plasma HIV RNA within 6 months after starting protease inhibitor therapy; multivariate analysis of risk factors for treatment failures. Results: A total of 226 treatment episodes with protease inhibitors were evaluable (saquinavir, 83; ritonavir, 47; indinavir, 96). The rate of virological treatment failure was 44% (saquinavir, 64%; ritonavir, 38%; indinavir, 30%). In a multivariate analysis, the following independent risk factors for virological failure were found: CD4 cell count, pretreatment with antiretroviral drugs (number), and protease inhibitor (compound). The relative risk reduction for each CD4 cell count increase was 0.997 (P = 0.012), 2.64 for pretreatment with one or two drugs versus no drug (P = 0.05), 2.97 for pretreatment with more than two drugs versus no drug (P = 0.05), and 4.62 for treatment with saquinavir versus indinavir (P = 0.001). Conclusion: An unexpectedly high rate of virological treatment failure of protease inhibitor therapy was found in an unselected cohort of HIV-infected patients. Response to antiretroviral combination therapy in normal clinical practice may considerably differ from results of randomized clinical trials. Further studies are warranted to find optimal treatment strategies for both initial and salvage therapy.
The effect of carbon dioxide on the sensitivity of Bacteroides fragilis to certain antibiotics in vitro

The effect of 10% carbon dioxide on the sensitivity to four antibiotics of 10 strains of Bacteroides fragilis was studied. The minimum inhibitory concentrations of erythromycin and lincomycin hydrochloride for these strains were four to 32 times higher, when grown in hydrogen plus 10% carbon dioxide, than the values obtained when the strains were grown in pure hydrogen. A similar effect was obtained by growing the strains in hydrogen on an acid medium. Except for Haemophilus influenzae and Clostridium tertium the sensitivity to erythromycin and lincomycin hydrochloride of other species of bacteria examined was not affected by the atmosphere in which the tests were carried out. 7-Chlorolincomycin and rifamycin B diethylamide, to which the strains of B. fragilis were uniformly sensitive, were not significantly affected by additional carbon dioxide. The possible mechanisms underlying this phenomenon and its clinical implications are discussed, and a case report describing the successful use of erythromycin in the treatment of a cerebral abscess due to B. fragilis is presented. In a recent study in this laboratory of the sensitivity to antibiotics of B. fragilis the majority of strains were found to be inhibited by 0·15 μg/ml of erythromycin and by 0·55 μg/ml of lincomycin hydrochloride (Ingham, Selkon, Codd, and Hale, 1968). After this work had been completed hydrogen plus 10% carbon dioxide was substituted for pure hydrogen in the anaerobic technique. Strains of B. fragilis isolated on routine culture now appeared to be relatively resistant to erythromycin and lincomycin hydrochloride when their sensitivity was examined by the disc diffusion method. A more detailed investigation of this phenomenon was carried out, the results of which are reported here. The opportunity was also taken to examine the susceptibility of B. fragilis to two new antibiotics, namely, 7-chlorolincomycin and rifamycin B diethylamide.
Disulfiram, an old drug with new potential therapeutic uses for human hematological malignancies

Disulfiram (DSF) is an aldehyde dehydrogenase inhibitor currently used for the treatment of alcoholism. Here, we show that multiple myeloma (MM) cell lines and primary cells from newly diagnosed and relapsed/resistant patients affected by MM, acute myeloid and lymphoblastic leukemia are significantly sensitive to DSF alone and in combination with copper. These effects are present at doses lower than those achievable in vivo after DSF standard administration. The cytotoxic effect achieved by this treatment is comparable to that obtained by conventional chemotherapy and is absent in normal hematopoietic cells. In addition, we found that DSF plus copper induces loss of mitochondrial membrane potential, triggers reactive oxygen species (ROS) production and activates executioner caspases. DSF‐copper‐induced apoptosis and caspases activation are strongly reversed by antioxidant N‐acetylcysteine, thus indicating a critical role of ROS. These results might suggest the use of the old drug DSF, alone or in combination with copper, in the treatment of hematological malignancies.
Ocular disorders in children in Zaria children's school.

BACKGROUND The main causes of blindness in children change over time. The prevalence and pattern of eye diseases in children were studied in northern Nigeria 6 years ago. This study like the previous one was a school eye health screening conducted in Zaria children school located at the centre of Zaria, a city in northern Nigeria. AIMS AND OBJECTIVES to determine the current prevalence and pattern of eye diseases affecting school children in Zaria. This is to serve as a current template for planning eye care for children in Zaria and environs. MATERIALS AND METHODS a cross sectional study of 327 children who completed a pre-designed school eye screening format was conducted. Consent was obtained from the school authority and the parents before the screening exercise. It involved assessment of visual acuity, anterior and posterior segment examination and colour vision testing. Intraocular pressure measurement and refraction were done for those with indications. RESULT A total of 327 children were examined, out of which 45.6% (n=149) were males and 54.4% (n=178) were females. M: F=1:1.2. Age range 5-17 yrs with mean of 9.6 ± 3.1(SD). The commonest causes of eye disorders were refractive errors 8.0% (n=26), allergic conjunctivitis 7.3 % (n=24), glaucoma suspects 3.7% (n=12) and colour deficiency 1.5%(n=5). CONCLUSION The major causes of childhood eye disorders were uncorrected refractive errors and allergic conjunctivitis. The predominance of uncorrected refractive error is similar to what is obtainable in other parts of the world especially in the urban areas.
Improved dissection efficiency in the human gross anatomy laboratory by the integration of computers and modern technology

The need to increase the efficiency of dissection in the gross anatomy laboratory has been the driving force behind the technologic changes we have recently implemented. With the introduction of an integrated systems‐based medical curriculum and a reduction in laboratory teaching hours, anatomy faculty at the University of North Texas Health Science Center (UNTHSC) developed a computer‐based dissection manual to adjust to these curricular changes and time constraints. At each cadaver workstation, Apple iMac computers were added and a new dissection manual, running in a browser‐based format, was installed. Within the text of the manual, anatomical structures required for dissection were linked to digital images from prosected materials; in addition, for each body system, the dissection manual included images from cross sections, radiographs, CT scans, and histology. Although we have placed a high priority on computerization of the anatomy laboratory, we remain strong advocates of the importance of cadaver dissection. It is our belief that the utilization of computers for dissection is a natural evolution of technology and fosters creative teaching strategies adapted for anatomy laboratories in the 21st century. Our strategy has significantly enhanced the independence and proficiency of our students, the efficiency of their dissection time, and the quality of laboratory instruction by the faculty. Clin. Anat. 17:337–344, 2004. © 2004 Wiley‐Liss, Inc.
The effect of peri‐conception hyperglycaemia and the involvement of the hexosamine biosynthesis pathway in mediating oocyte and embryo developmental competence

The environment that the oocyte is exposed to during the peri‐conception period can have a significant impact on oocyte developmental competence (the ability of the oocyte to support fertilisation and subsequent embryo development) and the long‐term health of the resulting offspring. This is particularly true for maternal hyperglycaemia. While maternal hyperglycaemia during early pregnancy through term development has been extensively studied, the effects on the oocyte itself, and the underlying mechanisms, remain largely unknown. There is increasing evidence, however, for the role of the fuel‐sensing hexosamine biosynthesis pathway in mediating the effects of hyperglycaemia in many different cell types. In this review, we will focus on the reproductive consequences of maternal hyperglycaemia during the peri‐conceptual period and the role of the hexosamine pathway in mediating these processes. Mol. Reprod. Dev. 81: ? –? , 2014. © 2014 Wiley Periodicals, Inc.
Prevalence of Cryptosporidium species in intensively farmed pigs in Ireland

SUMMARY Natural Cryptosporidium infections in pigs are widespread but generally apathogenic. This study was undertaken to determine the prevalence of zoonotic Cryptosporidium spp. in piggeries in Ireland, where the drinking water supply is particularly vulnerable to contamination with zoonotic species. Overall, infections were detected in 39 out of 342 animals (11·4%), with highest infection rates among weaners (15%) and sows (13·3%). Twenty-nine positive samples were genotyped based on SSU rRNA sequence analysis. Infections with Cryptosporidium parvum, the most important zoonotic species were rare and are likely to be of greater concern to animal handlers than suppliers of drinking water. In addition to C. parvum, Cryptosporidium suis, Cryptosporidium pig genotype II, Cryptosporidium muris and a previously undescribed genotype were identified. ABI-profiles indicated the presence of different alleles in at least 40% of all genotyped isolates. This was confirmed in 3 isolates by cloning of the PCR products. Since chronic mixed infections appear to be quite common in pigs they could be considered as models for mixed infections in immunocompromised humans.
Agonist‐stimulated divalent cation entry into single cultured human umbilical vein endothelial cells.

1. The free cytoplasmic Ca2+ concentration ([Ca2+]i) can be measured using Fura‐2 in superfused single human umbilical vein endothelial cells. When an endothelial cell is stimulated by a maximal dose of histamine (100 microM), [Ca2+]i rises to a peak and then falls back to a maintained plateau which is due to a stimulated Ca2+ influx. 2. If extracellular Ca2+ is replaced by 50 microM‐Mn2+ then 100 microM‐histamine causes a rise in [Ca2+]i accompanied by a fluorescence quench that signals the stimulated entry of Mn2+ into the cytoplasm. 3. If in Ca2(+)‐free solution a cell is stimulated by 100 microM‐histamine for 120 s to discharge the internal Ca2+ store, and then exposed to 50 microM‐Mn2+ after removal of the histamine, a similar stimulated Mn2+ entry is seen. This quench is unaffected by readdition of histamine and is not seen if the store is refilled by exposure to 1 mM‐extracellular Ca2+ for 180 s before exposure to the Mn2+. 4. The refilling of the internal store by exposure to 1 mM‐Ca2+ and the stimulated entry of Mn2+ are both blocked by 2 mM‐Ni2+. 5. If [Ca2+]i is stimulated to produce repetitive spikes by a low dose of histamine (0.3‐1 microM) in nominally Ca2(+)‐free solution containing Mn2+, then the stimulated quench is uniform and is not modulated by the [Ca2+]i spiking. 6. If the internal store is discharged by exposure to histamine in Ca2(+)‐free solution and then refilled for a short period then the cell is in a state where the internal store is partly full to an extent that depends on the duration of the refilling. In such an experiment, the rate of Mn2+ influx may be estimated by measuring the rate of quench during a short exposure to 50 microM‐Mn2+. The rate of Mn2+ entry varies inversely with the degree of fullness of the internal Ca2+ store. 7. If a similar experiment is repeated but with the fullness of the internal store being varied by varying the period of the initial exposure to 100 microM‐histamine, with no refilling, the same inverse relationship between Mn2+ influx and fullness of the internal store is obtained. 8. These experiments show that Mn2+ enters human umbilical vein endothelial cells following agonist stimulation by a pathway that is controlled by the degree of fullness of the internal store; it does not, however, enter the cytoplasm by exactly the same route as Ca2+. (ABSTRACT TRUNCATED AT 400 WORDS)
Engineering of vascular ingrowth matrices: Are protein domains an alternative to peptides?

Anastomotic intimal hyperplasia and surface thrombogenicity are the main reasons for the high failure rate of prosthetic small‐diameter vascular grafts. While anastomotic intimal hyperplasia is a multifactorial event, ongoing surface thrombogenicity is primarily caused by the lack of an endothelium, even after years of clinical implantation. After decades of poorly performing synthetic artery‐grafts, tissue engineering has emerged as a promising approach to generate biologically functional bio‐synthetic hybrid grafts mimicking native arteries regarding the presence of an endothelial lining on the blood surface. “In vitro endothelialization” represented the first generation of such tissue‐engineered vascular grafts, utilising cell culture techniques for the creation of a confluent autologous endothelium on ePTFE grafts. The clinical long‐term results with this method in almost 200 patients are highly encouraging, showing patencies equal to vein grafts. Since “in vitro endothelialization” requires cell culture facilities, it will always be confined to large centres. Therefore, research of the 1990s turned to the development of spontaneously endothelializing implants, to make tissue‐engineered grafts amenable to the entire vascular‐surgical community. Apart from scaffold designs allowing transmural ingrowth, biological signalling through a facilitating ingrowth matrix holds a key to spontaneous endothelialization. In biological signalling, the increasingly deeper understanding of bio‐active molecules and the discovery of domains and peptide sequences during the 1980s created the expectation in the 1990s that peptide signalling may be all that is needed. This present review highlights the possible problems associated with such a reductionist approach. Using the fibronectin molecule, we demonstrated that domains may be more suitable modules in tissue engineering than peptide sequences. Anat Rec 263:379–387, 2001. © 2001 Wiley‐Liss, Inc.
A Matched-control Follow-up and Family Study of ‘Puerperal Psychoses’

A hundred and ten women admitted to a psychiatric hospital within 90 days of childbirth were individually matched for age, psychiatric syndrome, and year of admission with women admitted to the same hospital with illnesses unrelated to childbirth. Both groups were followed up after a mean interval of nine years, and 72 matched pairs of patients for whom adequate information was obtained were then compared. The previous and subsequent psychiatric morbidity of these two groups, their subsequent obstetric careers, and the psychiatric morbidity of their first-degree relatives were all very similar. However, the puerperal women had significantly fewer relapses in the follow-up period, fewer committed suicide, and the psychiatric morbidity of their relatives tended to be lower. This better outcome was most marked in puerperal subjects with major depressions; those with manic disorders fared no better than controls. These results suggest that puerperal psychoses are basically the same as affective illnesses occurring at other times but, because childbirth is a uniquely potent precipitant of affective illness, some of those who develop puerperal episodes have a lesser genetic predisposition to affective illness than the generality of women with affective disorders.
Macrophage Migration Inhibitory Factor Up-regulates Matrix Metalloproteinase-9 and -13 in Rat Osteoblasts

Neutral matrix metalloproteinases (MMPs) play an important role in bone matrix degradation accompanied by bone remodeling. We herein show for the first time that macrophage migration inhibitory factor (MIF) up-regulates MMP-13 (collagenase-3) mRNA of rat calvaria-derived osteoblasts. The mRNA up-regulation was seen at 3 h in response to MIF (10 μg/ml), reached the maximum level at 6–12 h, and returned to the basal level at 36 h. MMP-13 mRNA up-regulation was preceded by up-regulation of c-jun and c-fos mRNA. Tissue inhibitor of metalloproteinase (TIMP)-1 and MMP-9 (92-kDa type IV collagenase) were also up-regulated, but to a lesser extent. The MMP-13 mRNA up-regulation was significantly suppressed by genistein, herbimycin A and 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine. Similarly, a selective mitogen-activated protein kinase (MAPK) kinase (MEK)1/2 inhibitor (PD98059) and c-jun/activator protein (AP)-1 inhibitor (curcumin) suppressed MMP-13 mRNA up-regulation induced by MIF. The mRNA levels of c-junand c-fos in response to MIF were also inhibited by PD98059. Consistent with these results, MIF stimulated phosphorylation of tyrosine, autophosphorylation of Src, activation of Ras, activation of extracellular signal-regulated kinases (ERK) 1/2, a MAPK, but not c-Jun N-terminal kinase or p38, and phosphorylation of c-Jun. Osteoblasts obtained from calvariae of newborn JunAA mice, defective in phosphorylation of c-Jun, or newborn c-Fos knockout (Fos−/−) mice, showed much less induction of MMP-13 with the addition of MIF than osteoblasts obtained from wild-type or littermate control mice. Taken together, these results suggest that MIF increases the MMP-13 mRNA level of rat osteoblasts via the Src-related tyrosine kinase-, Ras-, ERK1/2-, and AP-1-dependent pathway.
INDUCTION OF PYRIMIDINE DIMERS IN BACTERIAL DNA BY 365 nm RADIATION *

THE induction of pyrimidine dimers in bacterial DNA, both in uiuo and in uitro, by radiation of wavelengths as long as 3 13 nm is well established (Setlow and Carrier, 1966; Setlow, 1967) but little is known about the chemical nature of the damage induced by longer wavelengths. Oxygen-dependent lethal effects of 365 nm radiation have been demonstrated by Webb and Lorenz ( 19701, and indirect biological evidence suggests that at least part of the lethal damage is cyclobutane-type pyridimine dimers (Brown and Webb, 1972). In the experiments reported in this note, evidence is presented for the existence of pyrimidine dimers in the D N A of Escherichia coli irradiated at 365 nm.