Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histological and electron microscopic examinations of the kidneys of 8 dogs suffering from fatal, naturally acquired Babesia canis infection and nephropathy are presented. Seven animals were treated with imidocarb dipropionate on average 4.5 days prior to death. Severe anaemia was present only in 2 cases. Degenerative histological changes observed mostly in the proximal convoluted tubules included vacuolar-hydropic degeneration, necrosis and detachment of renal tubular epithelial (RTE) cells from the basement membrane. Necrotic debris occasionally formed acidophilic casts within the tubules. In some cases, necrosis of the whole tubule was observed. Haemoglobin casts in the tubules and haemoglobin droplets in RTE cells seldom appeared. No significant histological changes were seen in the glomeruli. Ultrastructural lesions in RTE cells included nuclear membrane hyperchromatosis, karyopyknosis, karyolysis, swelling or collapse of mitochondria with fragmentation of cristae and vacuolar-hydropic degeneration in the endoplasmic reticulum and microvilli. Nuclear oedema was also observed. Many RTE cells exhibiting necrosis collapsed. Vacuolar-hydropic degeneration and necrosis were also observed in the glomerular and interstitial capillary endothelium. The severe acute tubular necrosis described in this study is probably the result of hypoxic renal injury. Systemic hypotension leading to vasoconstriction in the kidneys might be the most important cause of renal hypoxia in B. canis infections, but anaemia may also contribute to inadequate oxygenation. Imidocarb should be applied with caution in patients with possible renal involvement until further data become available on its potential nephrotoxicity in dogs.
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PMID:Histological and ultrastructural studies of renal lesions in Babesia canis infected dogs treated with imidocarb. 1827 10

This study aimed at describing cerebral malaria cases findings in the Fann Hospital in Dakar. Data were collected from patients files recorded from 2001 to 2005. One hundred and twenty nine cases of cerebral malaria were admitted to the clinic, accounting for 21.4% of all malaria cases. The sex-ratio M/F was 2.48 and the mean age of patients 28.24 years old +/- 13.7 [12-85 years old]. Patients presented with either coma (91.4%) or mental confusion (10.07%) along with fever (80.6%), convulsions (33.3%). Other severe malaria conditions were observed: jaundice (7 cases), severe anaemia (5 cases), acute renal failure (3 cases), and circulatory collapse (3 cases). Acute pulmonary infection (4 cases) and Salmonella bacteraemia (2 cases) occurred as complications during patient's hospitalisation. The case fatality rate was 20.2% (26 deaths). No neurological sequelae were found among survivors. Cerebral malaria lethality is still high enough to urge for the improvement of working conditions in our clinic. Together with promotion of preventive measures in the community better health care services will help to reduce malaria related morbidity and mortality.
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PMID:[Cerebral malaria in adults at the Infectious Diseases Clinic in the Fann Hospital in Dakar, Senegal]. 1843 1

The removal of DNA interstrand cross-links (ICLs) has proven to be notoriously complicated due to the involvement of multiple pathways of DNA repair, which include the Fanconi anemia/BRCA pathway, homologous recombination and components of the nucleotide excision and mismatch repair pathways. Members of the SNM1 gene family have also been shown to have a role in mediating cellular resistance to ICLs, although their precise function has remained elusive. Here, we show that knockdown of Snm1B/Apollo in human cells results in hypersensitivity to mitomycin C (MMC), but not to IR. We also show that Snm1B-deficient cells exhibit a defective S phase checkpoint in response to MMC, but not to IR, and this finding may account for the specific sensitivity to the cross-linking drug. Interestingly, although previous studies have largely implicated ATR as the major kinase activated in response to ICLs, we show that it is activation of the ATM-mediated checkpoint that is defective in Snm1B-deficient cells. The requirement for Snm1B in ATM checkpoint activation specifically after ICL damage is correlated with its role in promoting double-strand break formation, and thus replication fork collapse. Consistent with this result Snm1B was found to interact directly with Mus81-Eme1, an endonuclease previously implicated in fork collapse. In addition, we also show that Snm1B interacts with the Mre11-Rad50-Nbs1 (MRN) complex and with FancD2 further substantiating its role as a checkpoint/DNA repair protein.
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PMID:Snm1B/Apollo mediates replication fork collapse and S Phase checkpoint activation in response to DNA interstrand cross-links. 1846 62

A 46-year-old non-obese woman with no previous history of pelvic surgery underwent a tension-free vaginal tape (TVT) procedure for the treatment of stress urinary incontinence. Perioperative cystoscopy revealed that both trocars had perforated the bladder. The procedure was cancelled due to excessive bleeding in the bladder, which impaired visibility by cystoscopy. Postoperatively the patient had increasing abdominal pain, anaemia and a tendency to collapse. Laparotomy was performed and, in addition to a haematoma in the retropubic space, 2 perforations were detected in the small intestine; these perforations were closed. Bowel perforations during TVT procedures are rare but sometimes fatal. They have been described in the literature and appear to be under-reported. Patients typically develop symptoms immediately after surgery, but some exceptional cases may develop symptoms after a few months. Bowel perforation should be considered when unexplainable symptoms arise after a minimally invasive procedure like TVT. Because this rare complication can be life-threatening, early recognition is very important.
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PMID:[Bowel perforation during placement of a tension-free vaginal tape for stress urinary incontinence]. 1854 29

A 68-year-old woman presented at the Casualty Department due to collapse, anaemia, fatigue and progressive dyspnoea. She suffered from melena, indicative of a haemorrhage in the upper gastrointestinal tract. Gastroduodenoscopy revealed the presence of a polyp in the duodenum, which was endoscopically resected. Pathological investigation demonstrated that the polyp was a Brunner's adenoma, i.e. a circumscript benign submucosal nodular hyperplasia of the Brunner's glands.
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PMID:[Melena associated with a Brunner's adenoma]. 1859 64

Defects in DNA repair pathways have been involved in collapse of early neurogenesis leading to brain development abnormalities and embryonic lethality. However, consequences of DNA repair defects in adult neural stem and progenitor cells and their potential contribution in ageing phenotype are poorly understood. The Fanconi anaemia (FA) pathway, which functions primarily as a DNA damage response system, has been examined in neural stem and progenitor cells during developmental and adult neurogenesis. We have shown that loss of fanca and fancg specifically provokes neural progenitor apoptosis during forebrain development, related to DNA repair defects, which persists in adulthood leading to depletion of the neural stem cell pool with ageing. In addition, neural stem cells from FA mice had a reduced capacity to self-renew in vitro. Here, we expand upon our recent work and give further data examining possible implication of oxidative stress. Therefore, FA phenotype might be interpreted as a premature ageing of stem cells, DNA damages being among the driving forces of ageing.
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PMID:Role of Fanconi DNA repair pathway in neural stem cell homeostasis. 1860 74

In 2006 an outbreak of canine distemper affected 14 young domestic ferrets in Barcelona, Spain. Their clinical signs included a reduced appetite, lethargy, dyspnoea, coughing, sneezing, mucopurulent ocular and nasal discharges, facial and perineal dermatitis, diarrhoea, splenomegaly and fever. Late in the course of the disease, general desquamation and pruritus, and hyperkeratotic/crusting dermatitis of the lips, eyes, nose, footpads, and perineal area were observed. None of the ferrets developed neurological signs. Non-regenerative anaemia and high serum concentrations of alpha- and beta-globulins were the most common laboratory findings. Most of the animals died or were euthanased because of respiratory complications. Postmortem there were no signs of lung collapse. Distemper was diagnosed by direct immunofluorescence of conjunctival swabs or pcr of several organs, and histology revealed the characteristic eosinophilic intracytoplasmic and intranuclear inclusion bodies of canine distemper virus in several organs. The minimum incubation periods calculated for six of the ferrets were 11 to 56 days, and in 13 of the ferrets the signs of disease lasted 14 to 34 days. Inclusion bodies compatible with infection by herpesvirus were found in the lungs of one of the ferrets.
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PMID:Outbreak of canine distemper in domestic ferrets (Mustela putorius furo). 1872 66

This study assessed the prevalence of trypanosomes in cattle at the Kachia Grazing Reserve (KGR) in March and June 2004 and in February 2005. A total of 1293 cattle blood samples were collected at random. The samples were analysed using the buffy coat technique and Giemsa thin blood films for parasite detection and identification. The effects of herd pen location to watering and grazing point's distances (using the global positioning system (GPS)) were determined and mean Packed cell volume (PCV) assessed. Overall, the detected prevalence of trypanosomosis was 8.4%, much higher than the previous prevalence of 5.3% before the present study was conducted. The prevalences in the months of March, June (2004) and February (2005) were 2.3%, 11.6% and 15.4%, respectively. Increased prevalence was associated with proximity of herd pens to watering point's distances (chi(2) for linear trend=4.447, P<0.05), but no association of herd pens to grazing point distances (chi(2)=2.186, P>0.05); suggesting that hydrological network played an important part in trypanosomosis transmission. The mean PCV of parasitaemic and apparasitaemic cattle were respectively 25.99+/-1.82% and 29.31+/-1.70%. The drop in mean PCV was most in 0-1-year age group, 23.47+/-3.10% and was statistically significant (P<0.05), suggesting that anaemia was most pronounced in this age group. Factors that may have contributed to the increased prevalence obtained were collapse of control measures and breed susceptibility. Since, Zebu cattle were the predominant breeds in the reserve, the study advocates effective use of insecticide impregnated screens (traps and targets) with community participation in mind for sustainability. If government intervenes through PATTEC ground spraying of insecticides in the reserve is recommended. In addition, chemotherapeutic and chemoprophylaxis should be systematically used to fight the problem of trypanosomosis in the KGR towards improved livestock production.
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PMID:Survey of bovine trypanosomosis in the Kachia Grazing Reserve, Kaduna State, Nigeria. 1910 Oct 87

Elaborate processes act at the DNA replication fork to minimize the generation of chromatid discontinuity when lesions are encountered. To prevent collapse of stalled replication forks, mutagenic translesion synthesis (TLS) polymerases are recruited temporarily to bypass DNA lesions. When a replication-associated (one-ended) double-strand break occurs, homologous recombination repair (HRR) can restore chromatid continuity in what has traditionally been regarded as an "error-free" process. Our previous mutagenesis studies show an important role for HRR in preventing deletions and rearrangements that would otherwise result from error-prone nonhomologous end joining (NHEJ) after fork breakage. An analogous, but distinct, role in minimizing mutations is attributed to the proteins defective in the cancer predisposition disease Fanconi anemia (FA). Cells from FA patients and model systems show an increased proportion of gene-disrupting deletions at the hprt locus as well as decreased mutation rates in the hprt assay, suggesting a role for the FANC proteins in promoting TLS, HRR, and possibly also NHEJ. It remains unclear whether HRR, like the FANC pathway, impacts the rate of base substitution mutagenesis. Therefore, we measured, in isogenic rad51d and fancg CHO mutants, mutation rates at the Na(+)/K(+)-ATPase alpha-subunit (ATP1A1) locus using ouabain resistance, which specifically detects base substitution mutations. Surprisingly, we found that the spontaneous mutation rate was reduced approximately 2.5-fold in rad51d knockout cells, an even greater extent than observed in fancg cells, when compared with parental and isogenic gene-complemented control lines. A approximately 2-fold reduction in induced mutations in rad51d cells was seen after treatment with the DNA alkylating agent ethylnitrosurea while a lesser reduction occurred in fancg cells. Should the model ATP1A1 locus be representative of the genome, we conclude that at least 50% of base substitution mutations in this mammalian system arise through error-prone polymerase(s) acting during HRR-mediated restart of broken replication forks.
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PMID:RAD51D- and FANCG-dependent base substitution mutagenesis at the ATP1A1 locus in mammalian cells. 1942 12

We conducted this study to find out the incidence of extubation failure (EF) in ventilated neonates and associated clinical risk factors. Eighty two ventilated neonates were followed up to 48 hours post extubation to look for EF. Twenty two babies (26.8%) had EF. The common risk factors for EF were presence of patent ductus arteriosus, post-extubation lung collapse and acquired pneumonia. The duration of ventilation, and maximum and pre-extubation alveolar arterial oxygen gradients (AaDO2) were significantly higher (P<0.05) in EF group. The incidence of sepsis (P=0.034), anemia (P=0.004) and pneumonia (P=0.001) were significantly higher in EF group. Detection of significant PDA and adequate post extubation care may help to reduce rate of extubation failure in neonates.
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PMID:Clinical risk factors associated with extubation failure in ventilated neonates. 1943 70


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