Full-length ureteric splintage in the management of bilharzial ureteric strictures

Our experience with full-length ureteric splintage is reviewed with a note on the technique and its outcome. It is safe, effective and simple, easy to teach and easy to learn. It is recommended as the operation of choice in bilharzial ureteropathy.     

Rapid Progression of Native Renal Artery Fibromuscular Dysplasia Following Kidney Donation

Fibromuscular dysplasia is the second commonest anatomical abnormality apart from multiple renal arteries in the potential live donors. Pretransplant evaluation of the donors may include an angiography to evaluate the renal arteries, and failure to recognize renal arterial stenosis, particularly fibromuscular dysplasia, by noninvasive methods may eventually lead to hypertension and ischemic renal failure. We report a case of fibromuscular dysplasia that was undetected by computed tomographic angiography prior to donation. One year after kidney donation, it rapidly progressed to severe symptomatic stenosis with hypertension and acute renal failure. Following renal artery angioplasty, her blood pressure normalized over a period of 2 weeks without any need for antihypertensive medications and the serum creatinine returned to her baseline. The acceptability of renal donors with fibromuscular dysplasia depends on the age, race and the availability of the other suitable donors. Mild fibromuscular dysplasia in a normotensive potential renal donor cannot be considered a benign condition. Such donors need regular follow-up postdonation for timely detection and treatment.     

Bench-to-bedside review: Resuscitation in the emergency department

Over the past decade the practice of acute resuscitation and its monitoring have undergone significant changes. Utilization of noninvasive mechanical ventilation, goal-directed therapy, restricted fluid volume, blood transfusion and minimally invasive technology for monitoring tissue oxygenation have changed the practice of acute resuscitation. Early diagnosis and definitive treatment of the underlying cause of shock remains the mainstay for survival after successful resuscitation. Patient-centered outcome end-points, in addition to survival, are being utilized to appraise the effectiveness of treatment. Application of medical ethics to the ever changing practice of acute resuscitation has also become a societal expectation.     

Gastrinomas demonstrate amplification of the HER-2/neu proto-oncogene.

OBJECTIVE: This study determined whether genomic amplification of HER-2/neu or mutations of the p53 and ras genes were present in gastrinomas. SUMMARY BACKGROUND DATA: Amplification of HER-2/neu, a proto-oncogene related to the epidermal growth factor receptor, and mutation of the ras proto-oncogene and p53 tumor suppressor gene appear to play a role in the pathogenesis of some human cancers. Little is known about possible molecular alterations in gastrinomas, tumors that may be particularly virulent because of gastrin overproduction, resulting in the severe ulcer diathesis, the Zollinger-Ellison syndrome. METHODS: The differential polymerase chain reaction (PCR) procedure was used to detect amplification of the HER-2/neu gene in DNA samples from the novel human gastrinoma cell line (PT) and from paraffin-embedded samples of gastrinomas. Sequencing techniques were used to determine whether mutations of the p53 or ras (Ha-ras, N-ras, Ki-ras) genes were present. RESULTS: Amplification (> twofold) occurred in all gastrinoma tumor samples. Compared with normal pancreas or ileum, a 4- to 12-fold amplification of HER-2/neu was found in 3 gastrinomas, 3 to 3.3-fold in four samples and 2.1- to 2.4-fold in the remaining five tumors. A heterozygous point mutation in the p53 gene (codon 273) was found in a single sample; none of the gastrinomas contained a mutation of the ras genes. CONCLUSIONS: Amplification of the HER-2/neu gene, but not alterations of either p53 or ras, may be involved in the pathogenesis of gastrinomas. The unique PT cell line will be a useful model to further elucidate the molecular mechanisms that contribute to gastrinoma formation and growth.     

In vitro effect of alpha-interferon on mononuclear cells of normal and autoimmune patients

The effect of lymphoblastoid interferon (IFN-alpha) on cell-mediated and humoral immunity was studied in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). The base-line natural killer (NK) and antibody dependent cytotoxic cell (ADCC) activity was higher than normal in individuals with RA. The NK and ADCC activities were tested after IFN-alpha pretreatment and the augmentation of NK and ADCC activity was less in these patients than in normals. Lymphoblastoid IFN inhibited antigen induced T-cell proliferation in SLE to a lesser extent than in normal individuals. Finally, the addition of lymphoblastoid IFN was also less effective at suppressing in vitro polyclonal antibody formation by mononuclear cells from patients with SLE than from normals, with enhancement observed in some patients at the lower IFN-alpha concentrations tested.     

Loss of lymphocyte chalone activity in mice with autoimmune disease.

Lymphocyte chalone from the spleens of old BALB/c, young BALB/c and young NZB mice caused significant suppression of the proliferative response of BALB/c and NZB spleen cells to T and B mitogens, whereas lymphocyte chalone from old NZB spleen did not suppress. Lymphocyte chalone from young and old NZB mice was tested using different ages of NZB/NZW responding spleen cells; at all ages concanavalin A- and lipopolysaccharide-induced proliferation was suppressed less by the chalone from old NZB mice than from that of young NZB mice. The responding NZB/NZW cells were suppressed equivalently at all ages studied. The basis for the loss of lymphocyte chalone activity in old NZB mice remains unknown; however, it appears likely that this event has a role in the disturbance of the negative feedback control system which contributes to NZB autoimmune disease.     

The Effect of Neonicotinoids Exposure on Oreochromis niloticus Histopathological Alterations and Genotoxicity

This study aimed to examine the side effects of selected neonicotinoids (Acetamiprid, Aceta, and Imidacloprid, Imid) on Oreochromis niloticus juveniles. The acute toxicity, Probit method, revealed an LC₅₀ of 195.81 and 150.76 ppm for Aceta/96 h and Imid/72 h respectively. The fish were divided into three groups that were exposed, for 21 days (n?=?5/replicate), to 1/10 of the LC₅₀ of either neonicotinoids, however, the third was an unexposed control group. Results of erythrocytic micronucleus (MN), and nuclear abnormalities (NA) showed that Aceta and Imid exposure caused a significant (p?<?0.05) increase in MN by?~?2.2 and?~?10 folds, respectively relative to control. NAs occurred at the order of kidney-shaped?>?budding?>?binucleated in Aceta, however, budding?>?binucleated?>?kidney-shaped was noticed in the Imid group. Histopathological changes in gills, liver, and muscles were observed significantly in both exposed groups with more severity in the Imid group. Collectively, Aceta and Imid have potential genotoxicity and histopathological alterations in O. niloticus.