Esophageal and gastric dysmotility in non ulcer dyspepsia.

BACKGROUND: The pathophysiology of non ulcer dyspepsia is poorly understood. Data on gastrointestinal motility alterations in this condition in the Indian population are scanty. We studied esophageal and gastric motility in patients with non ulcer dyspepsia. METHODS: 58 consecutive patients with non ulcer dyspepsia (according to the Rome criteria) were studied; 10 healthy volunteers were studied as controls. Esophageal transit of solid and liquid boluses (in all patients) and solid-phase gastric emptying (in 20 patients) were studied using scintigraphic techniques. RESULTS: Delayed esophageal transit and delayed gastric emptying were observed in 32 (55%) and 9 (45%) patients, respectively. Delay of both esophageal and gastric transit was found in 5 patients. Mean (SD) esophageal transit for liquid bolus was significantly delayed in patients (9.3 [3.7] s) compared to controls (7.0 [2.0] s; p < 0.01). Mean (SD) gastric emptying time (T50) was significantly delayed in patients (61.6 [13.6] min) compared to controls (50.0 [5.0] min; p < 0.001). Esophageal and gastric delayed transit was found in about two thirds of patients with dysmotility-like dyspepsia, but there were no significant difference in these abnormalities among different subgroups of dyspepsia. CONCLUSION: High prevalence of esophageal and gastric transit delay was found in non ulcer dyspepsia, particularly in the dysmotility subgroup.     

Identification of the prooxidant site of human ceruloplasmin: A model for oxidative damage by copper bound to protein surfaces

Free transition metal ions oxidize lipids and lipoproteins in vitro; however, recent evidence suggests that free metal ion-independent mechanisms are more likely in vivo. We have shown previously that human ceruloplasmin (Cp), a serum protein containing seven Cu atoms, induces low density lipoprotein oxidation in vitro and that the activity depends on the presence of a single, chelatable Cu atom. We here use biochemical and molecular approaches to determine the site responsible for Cp prooxidant activity. Experiments with the His-specific reagent diethylpyrocarbonate (DEPC) showed that one or more His residues was specifically required. Quantitative [¹⁴C]DEPC binding studies indicated the importance of a single His residue because only one was exposed upon removal of the prooxidant Cu. Plasmin digestion of [¹⁴C]DEPC-treated Cp (and N-terminal sequence analysis of the fragments) showed that the critical His was in a 17-kDa region containing four His residues in the second major sequence homology domain of Cp. A full length human Cp cDNA was modified by site-directed mutagenesis to give His-to-Ala substitutions at each of the four positions and was transfected into COS-7 cells, and low density lipoprotein oxidation was measured. The prooxidant site was localized to a region containing His⁴²⁶ because Cp_H426A almost completely lacked prooxidant activity whereas the other mutants expressed normal activity. These observations support the hypothesis that Cu bound at specific sites on protein surfaces can cause oxidative damage to macromolecules in their environment. Cp may serve as a model protein for understanding mechanisms of oxidant damage by copper-containing (or -binding) proteins such as Cu, Zn superoxide dismutase, and amyloid precursor protein.     

Normal cellular counterparts of B cell chronic lymphocytic leukemia

In an attempt to compare B cell chronic lymphocytic leukemia (B-CLL) with its normal cellular counterpart, the cell surface phenotype of 100 cases of B-CLL was determined by using a panel of monoclonal antibodies (MoAbs) directed against B cell-restricted and -associated antigens. The majority of B-CLL cells expressed Ia, B4 (CD19), B1 (CD20), B2 (CD21), surface immunoglobulin (sIg), and T1 (CD5) but lacked C3b (CD35) receptors. In contrast, the overwhelming majority of small unstimulated B cells expressed Ia, B4, B1, B2, sIg, and C3b receptors but lacked detectable T1. Small numbers of weakly sIg+ cells could be identified in peripheral blood and tonsil that coexpressed the B1 and T1 antigens. Approximately 16% of fetal splenocytes coexpressed B1, T1, weak sIg, B2, and Ia but lacked C3b receptors and therefore closely resembled most B-CLL cells. With the phenotypic differences between the majority of small unstimulated B cells and B-CLL cells, we examined normal in vitro activated B cells and B-CLL cells for the expression of B cell-restricted and -associated activation antigens. Of 20 cases examined, virtually all expressed B5, and approximately 50% of the cases expressed interleukin-2 receptors (IL-2R) and Blast-1. Normal B cells were activated with either anti-Ig or 12-0-tetradecanoylphorbol- beta-acetate (TPA) and then were examined for coexpression of B1, T1, and the B cell activation antigens B5 and IL-2R. Only cells activated with TPA coexpressed B1 and T1 as well as B5 and IL-2R. B cells activated with either anti-Ig or TPA proliferated in the presence of IL- 2, whereas B-CLL cells did not, although they all expressed the identical 60-kilodalton proteins by immunoprecipitation. These studies are consistent with the notion that B-CLL resembles several minor subpopulations of normal B cells including a population of B cells that are activated in vitro directly through the protein kinase C pathway.     

Students' expectations of postregistration degree programmes

The needs of postregistration students pursuing degree-linked clinical courses have received little attention and there are few insights concerning their aspirations when they enrol on such courses. Thus the aim of this study was to explore postregistration students' perceptions of the specific needs of their patient/client group and to examine how they envisaged the course on which they had just enrolled might help them to meet these needs in addition to their own requirements for professional and personal development. Data were collected by group interview from 62 students enrolling on eight different postregistration courses, all employed in an acute hospital trust. The results were analysed inductively. They indicated that students had internalized the state of the healthcare market and were keenly aware of the need to fulfil the expectations of employers and the public, while fulfilling their own needs for education and pursuing their own professional and career trajectories. They appeared ambitious and yet appeared to demonstrate empathy for patients and their families and felt a tremendous desire to provide care of a high quality through the optimal development of technical expertise. Students' emphasis on the importance of keeping abreast of technological developments should not be lightly dismissed considering its prominent position within the acute areas where they were employed, especially as it did not replace their desire to promote the caring aspects of their work.     

Biological,chemical and pharmacological aspects of Madhuca longifolia

Madhuca longifolia(M. longifolia) is also known as Mahua belonging to the family sapoteace family. M. longifolia is used in traditional and folklore system of medicine widely across India, Nepal, and Sri Lanka for its various pharmacological properties as in snake bites and in diabetes. Phytochemicals studies documented the different bioactive constituents, namely,glycosides, flavonoids, terpenes and saponins. The pharmacological studies proved that it possess wide range of biological activities such as antiulcer, antiinflammatory, antioxidant and antidiabetic activities. The toxicity studies reveal its non-toxic effect even at larger doses.Thus M. longifolia can be considered as a therapeutic agent for specific diseases. Scientific investigation on various isolated bioactive components and its efficacy on diseases proved the future usefulness of different species of Madhuca. This review summarizes the phytochemical,pharmacological, medicinal and non-medicinal uses of M. longifolia. Further exploration on M.longifolia for its therapeutic potential is however required for depth traditional knowledge.     

Fournier Gangrene from a Thirty-Two-Centimeter Rectosigmoid Foreign Body

Background

Medical and surgical problems associated with rectal foreign bodies are rare. Although most rectal foreign bodies can be removed without subsequent sequelae, they pose significant risk of infection.

Objectives

We report a patient with a 32-cm rectosigmoid foreign body and subsequent development of Fournier gangrene despite successful removal of the foreign body.

Case Report

A 63-year-old Caucasian man with past medical history of diabetes mellitus and depression presented with a chief complaint of “something stuck in my intestine.” He admitted that he placed a foreign body in the rectum. Abdominal X-ray study and computed tomography of the abdomen/pelvis showed a conical-shaped 32-cm rectosigmoid foreign body. The foreign body was removed manually and follow-up colonoscopy was done. The patient's condition deteriorated in the first 2 days of hospital stay and he was diagnosed with Fournier gangrene. He required multiple surgeries and received broad-spectrum antibiotic coverage for mixed bacterial flora grown from deep tissue.

Conclusion

Rectal foreign bodies can cause Fournier gangrene. A close observation and follow-up is important after removal of rectal foreign bodies.     

Primary Ewing sarcoma: follow-up with Ga-67 scintigraphy

While avid accumulation of gallium-67 citrate and technetium-99m methylene diphosphonate (MDP) occurs initially in most cases of primary Ewing sarcoma, uptake after therapy is less well defined. Thirty patients with Ewing sarcoma who underwent Ga-67 and bone scintigraphy at diagnosis, at completion of therapy, and at relapse from 1978 to 1988 were evaluated. All 30 patients showed less primary site Ga-67 activity following therapy. Twenty-three of 28 patients who underwent corresponding bone scintigraphy showed less uptake, but residual activity was usually more intense than with Ga-67. Avid reaccumulation of Ga-67 occurred in four of five patients with primary site relapse, while patients who underwent bone scintigraphy showed less change. It was concluded that a greater decrease in Ga-67 than in Tc-99m MDP uptake often occurs in patients successfully treated for primary Ewing sarcoma. Information obtained at Ga-67 scintigraphy is most likely to be helpful if results of bone scintigraphy remain abnormal or if occult relapse is suspected.     

Arsenic and liver disease.

The hepatotoxic action of arsenic, when used as a therapeutic agent, has long been recognised. Data on liver involvement following chronic exposure to arsenic-contaminated water are scanty. The nature and degree of liver involvement are reported on the basis of hospital based studies in patients who consumed arsenic contaminated drinking water for one to 15 years. Two hundred forty-eight patients with evidence of chronic arsenic toxicity underwent clinical and laboratory examination including liver function tests and hepatitis B surface antigen (HBsAg) status. Liver biopsy was done in 69 cases; in 29 patients, liver arsenic content was estimated by neutron activation analysis. Hepatomegaly was present in 190 of 248 patients (76.6%). Non-cirrhotic portal fibrosis was the predominant lesion (91.3%) in liver histology. The maximum arsenic content in liver was 6 mg/kg (mean 1.46 [0.42], control value 0.16 [0.04]; p <0.001); it was undetected in 6 of 29 samples studied. The largest number of patients with liver disease due to chronic arsenicosis from drinking arsenic contaminated water are reported. Non-cirrhotic portal fibrosis is the predominant lesion in this population. Hepatic fibrosis has also been demonstrated due to long term arsenic toxicity in an animal model. Initial biochemical evidence of hepatic membrane damage, probably due to reduction of glutathione and antioxidant enzymes, may be seen by 6 months. Continued arsenic feeding resulted in fatty liver with serum aminotransferases elevated at 12 months and hepatic fibrosis at 15 months.