Pattern of upper gastrointestinal haemorrhage in northern India—An endoscopic study of 316 patients

Three hundred and sixteen patients with acute upper gastrointestinal haemorrhage were studied prospectively and consecutively. The most frequent cause was variceal bleeding due to portal hypertension (36%), followed by peptic ulceration (24%) and gastric erosions (19%). Variceal haemorrhage tended to be severe and had a high individual mortality rate. Associated acute mucosal lesions with portal hypertension were strikingly less frequent when compared with the experience from the West. Seven per cent of patients died of bleeding alone and an equal number of an associated systemic disorder or complication. Splenomegaly was present in all patients with a variceal haemorrhage due to non-cirrhotic portal hypertension. However, in patients with portal hypertension due to cirrhosis splenomegaly was present in 63%. Endoscopy altered the clinical diagnosis in 13.2% of patients. Based on previous experience oesophago-gastro-duodenal endoscopy has been a useful tool in the management of acute upper gastrointestinal haemorrhage.     

B VITAMIN DEFICIENCY AND NEUROPSYCHIATRIC SYNDROMES IN ALCOHOL MISUSE

Alcohol misuse and alcohol withdrawal are associated with avariety of neuropsychiatric syndromes, some of which are associatedwith significant morbidity and mortality B vitamin deficiencyis known to contribute to the aetiology of a number of thesesyndromes, and B vitamin supplementation thus plays a significantpart in prophylaxis and treatment. In particular, the Wernicke-Korsakoffsyndrome (WKS), due to thiamine deficiency, is a common conditionin association with alcohol misuse, and is associated with highmorbidity and mortality. Nicotinamide deficiency may resultin a rarer condition, alcoholic pellagra encephalopathy, whichoften has a similar clinical presentation to WKS. This reviewconsiders the role of B vitamins in the aetiology and treatmentof neuropsychiatric syndromes associated with alcohol misuse,with particular emphasis on WKS.     

Treatment Patterns and Cost of Nonmelanoma Skin Cancer Management

INTRODUCTION: Nonmelanoma skin cancer (NMSC) is the most common form of cancer in the United States, more common than all other cancers combined. The factors that affect the cost of skin cancer management are not well defined. OBJECTIVE: The objective was to estimate cost of episodes of NMSC care and the factors that impact those costs. DESIGN: Medicare Current Beneficiary Survey (MCBS) data from 1999 to 2000 were used to assess costs of episodes of NMSC care. MCBS estimates of the number of episodes occurring in three service settings (physician's office, outpatient/ambulatory surgical center, or hospital) and demographics were obtained. RESULTS: There were 497 episodes of care in 372 patients. Half the episodes were treated by dermatologists, and two-thirds were managed in physicians' offices. The mean episode cost for management in the office setting was 500 dollars (SD, +/- 487 dollars), and costs were higher when the episodes were treated in either the ambulatory surgical center or the hospital settings, 935 dollars (SD, +/- 456 dollars) and 4,345 dollars (SD, +/- 4939 dollars), respectively. CONCLUSION: With the rising incidence and cost of NMSC to Medicare, it is increasingly important to preserve the low-cost management of this disease. Maintaining care of NMSC in the office-based setting is more cost-efficient than utilizing ambulatory surgical centers or hospital operating rooms.     

Hematological Observations on the Anemia Associated with Blood Type Rhnull

The purpose of this report is to direct attention of hematologists to a mild chronichemolytic anemia, of unexplained etiology, characterized by the remarkableabsence of all Rh-Hr factors. There arealso defects in the Ss, U blood group determinants. The anemia has most of theroutine hematological characteristics ofmild stomatocytosis and/or hereditaryspherocytosis. Like hereditary spherocytosis, it shows no abnormalities of intraerythrocytic enzymes nor of membranelipids. Unlike hereditary spherocytosis,however, its inheritance is recessive. Theproposed basis for this hemolytic anemiais homozygosity for a gene whose normalallele produces components of the erythrocyte membrane which function in themaintenance of intracellular osmoticequilibrium and which serves as substratefor the action of both the products of theRh-Hr genes and of the genes of theMNSs, U and, possibly, of the Fy systems.

Submitted on November 19, 1969 Revised on February 3, 1970 Accepted on February 17, 1970     

Overview of Developmental Heart Defects by Dioxins,PCBs, and Pesticides

The developing cardiovascular system is a sensitive target of many environmental pollutants, including dioxins, dioxin-like polychlorinated biphenyls (PCBs), and some pesticides such as methyl parathion. Laboratory research has utilized a variety of vertebrate models to elucidate potential mechanisms that mediate this cardioteratogenicity and to establish the sensitivity of different species for predicting potential risk to environmental and human health. Studies of dioxin and dioxin-like PCBs have illustrated that piscine, avian, and mammalian embryos exhibit cardiovascular structural changes and functional deficits, although the specific characteristics vary among the individual models. Piscine models typically exhibit reduced blood flow, altered heart looping, and reduced heart size and contraction rate. The chick embryo exhibits extensive cardiac dilation, thinner ventricle walls, and reduced responsiveness to chronotropic stimuli, while the murine embryo exhibits reduced heart size. It is notable that in all models the dioxin-associated cardioteratogenicity is associated with increases in cardiovascular apoptosis and decreases in cardiocyte proliferation. While the cardiotertogenicity in piscine and avian species is associated with overt morbidity and mortality, that is not the case for the murine embryo. However, murine offspring exposed during development to dioxin exhibit cardiac hypertrophy and an increased sensitivity to a second cardiovascular insult in adulthood. Thus, although the mammalian embryo is less sensitive to cardiovascular defects by dioxin and dioxin-like compounds, developmental exposure increases the risk of cardiovascular disease later in life. The impact of developmental exposure to dioxin-like chemicals on human cardiovascular disease susceptibility is not known. However, recent animal research has confirmed human epidemiology studies that dioxin exposure in adulthood is associated with hypertension and cardiovascular disease.     

Unrelated donor bone marrow transplantation for children and adolescents with aplastic anaemia or myelodysplasia

Allogeneic transplantation from an HLA-matched family member has been shown to be effective in reconstituting normal haemopoiesis in young people with severe cytopenias, classified as myelodysplastic syndrome (MDS) or severe aplastic anaemia (SAA). Unrelated donor transplant is a therapeutic choice for patients without a suitable family member donor. We report the outcome of seven patients < 20 years old with SAA and 10 with MDS treated with BMT from an HLA A,B DRB1 matched ( n  =8) or A or B locus mismatched ( n  =9) unrelated donor at the University of Minnesota between March 1988 and August 1995. Primary graft failure occurred in two patients and secondary graft failure in one, who was subsequently successfully engrafted with a second donor marrow infusion. Grades II–IV GVHD occurred in 10/16 (63%), and grades III–IV in 6/16 (37%) evaluable patients. Nine of the 17 patients (six with MDS and three with SAA) survive with full donor chimaerism, a median of 1.2 years post-BMT (range 3 months to 7 years). We recommend early referral for consideration of unrelated donor BMT for young patients with MDS, and patients with SAA without response to immunosuppression.     

The treatment of normospermic infertility by gamete intrafallopian transfer (GIFT)

Summary. Gamete intrafallopian transfer (GIFT) was applied in 207 treatment cycles in 73 couples. The pregnancy rate in cycles with only one (2/21, 9·5%) or two (2/29, 6·9%) oocytes transferred was significantly less than that in which four oocytes (36/116, 31·0%) were replaced. The collection of more than four oocytes did not influence the pregnancy rate in that treatment cycle. The overall pregnancy rate was 24·2% (50 of 207) and was similar in the four infertility groups studied (non-occlusive tubal disorders, endometriosis, cervical factor and unexplained infertility) with 28 (56%) of the pregnancies delivered at 20 weeks. The pregnancy wastage included 4 (8%) ectopic pregnancies and 3 (6%) late pregnancy losses. The 12 multiple pregnancies occurred following the transfer of three and four oocytes.     

Therapeutic and Diagnostic Benefits of Intentional Crosstalk Mediated Ventricular Output Inhibition

Ventricular output inhibition due to crosstalk is generally considered unsafe and something that should be avoided. Special circuits have been incorporated in some dual chamber pacing systems to absolutely prevent this from happening. However, in patients with intact atrioventricular conduction, crosstalk mediated ventricular output inhibition can be beneficial to the evaluation and management of the patient. Utilizing this technique, one can achieve single chamber atrial paced rates which greatly exceed the rates allowed by lower rate limit programming to facilitate an assessment of the integrity of AV nodal conduction and to both convert and suppress some pathological tachyarrhythmias. The methods of achieving crosstalk and its utilization in four patients is discussed in this report.     

The neurofilament antibody RT97 recognises a developmentally regulated phosphorylation epitope on microtubule-associated protein 1B

Microtubules are important for the growth and maintenance of stable neuronal processes and their organisation is controlled partly by microtubule-associated proteins (MAPs). MAP 1B is the first MAP to be expressed in neurons and plays an important role in neurite outgrowth. MAP 1B is phosphorylated at multiple sites and it is believed that the function of the protein is regulated by its phosphorylation state. We have shown that the monoclonal antibody (mAb) RT97, which recognises phosphorylated epitopes on neurofilament proteins, fetal tau, and on Alzheimer's paired helical filament-tau, also recognises a developmentally regulated phosphorylation epitope on MAP 1B. In the rat cerebellum, Western blot analysis shows that mAb RT97 recognises the upper band of the MAP 1B doublet and that the amount of this epitope peaks very early postnatally and decreases with increasing age so that it is absent in the adult, despite the continued expression of MAP 1B in the adult. We confirmed that mAb RT97 binds to MAP 1B by showing that it recognises MAP 1B immunoprecipitated from postnatal rat cerebellum using polyclonal antibodies to recombinant MAP 1B proteins. We established that the RT97 epitope on MAP 1B is phosphorylated by showing that antibody binding was abolished by alkaline phosphatase treatment of immunoblots. Epitope mapping experiments suggest that the mAb RT97 site on MAP 1B is near the N-terminus of the molecule. Despite our immunoblotting data, immunostaining of sections of postnatal rat cerebellum with mAb RT97 shows a staining pattern typical of neurofilaments with no apparent staining of MAP 1B. For instance, basket cell axons and axons in the granule cell layer and white matter stained, whereas parallel fibres did not. These results suggest that the MAP 1B epitope is masked or lost under the immunocytochemical conditions in which the cerebellar sections are prepared. The upper band of the MAP 1B doublet is believed to be predominantly phosphorylated by proline-directed protein kinases(PDPKs). PDPKs are also good candidates for phosphorylating neurofilament proteins and tau and therefore we postulate that the sites recognised by RT97 on these neuronal cytoskeletal proteins may be phosphorylated by similar kinases. Important goals are to determine the precise location of the RT97 epitope on MAP 1B and the kinase responsible.