Histopathological analysis of hysterectomy specimens

The objective of this study was to explore the histopathological findings and the rate of removal of ovaries in hysterectomy specimens. This study took into account 328 hysterectomy specimens examined in the Department of Pathology, Mymensingh Medical College and in one private Pathology Laboratory in Mymensingh town from March to August, 2005. Formalin fixed paraffin embedded tissue sections stained with haematoxylin and eosin were examined under light microscope. Patients' age, parts of uterus examined and their histopathological findings were retrieved from laboratory records. The common histopathological findings were: chronic cervicitis (87.80%), leiomyoma (17.07%), uterine prolapse (16.72%), adenomyosis (3.96), non-specific endometritis (3.35%), squamous cell carcinoma of cervix (2.44%), endometrial polyp (2.44%), serous cystadenoma of ovary (2.44%) and endometrial hyperplasia (1.83%). Some of the specimens show more than one lesions in the body of uterus, of which coexistence of adenomyosis and leiomyoma was the most common. Neoplastic lesions in cervix were 4.27%, in body 16.92% and in ovaries 5.06%. Malignant neoplasms were found in cervix 71.43%, in uterine corpus 3.03% and in ovaries 25%. Ovaries of both sides were removed in 48.17% of total cases. Their median age was 45 years, lowest age 23 years and maximum age was 82. The rate of removal of both ovaries was found to be increasing with the increase of age. Only one case was found to be subtotal hysterectomy and others were total hysterectomy. The present study revealed that the most common histopathological cause of hysterectomy is chronic cervicitis. Most common neoplastic cause of hysterectomy is leiomyoma. The rationalities and the possible after effect of hysterectomy in sexual functions and other physiological impairment should be followed up.     

T2182C mutation in 23S rRNA is associated with clarithromycin resistance in Helicobacter pylori isolates obtained in Bangladesh

Twelve clarithromycin-resistant (MIC, > or = 1 microg/ml) Helicobacter pylori isolates were analyzed for point mutations in the 23S rRNA gene. Sequence analysis of all of the resistant isolates revealed a T-to-C transition mutation at position 2182. Transformation experiments confirmed that a single T-to-C transition mutation at position 2182 is associated with clarithromycin resistance.     

Vasoactive agents modulate migration of monocytes across glomerular endothelial cells.

BACKGROUND: Macrophages seem to play an important role in the development of glomerulosclerosis. In both human and experimental animal models of focal glomerulosclerosis (FSGS), infiltration of macrophages in the mesangium has been considered key in the development of FSGS. METHODS: In the present study, we evaluated the effect of vasoactive agents on the migration of monocytes across a filter in a modified Boyden chamber as well as across a cultured glomerular endothelial cell layer (in vitro model of glomerular mesangium). Both light as well as scanning electron microscopic studies were performed. We evaluated the effect of vasoactive agents including histamine, prostaglandin (PG) E2, angiotensin II, endothelin-1, platelet-activating factor, and interleukin-1 (IL) on the migration of monocytes/macrophages across an endothelial cell layer as well as a gelatin-coated filter. In addition, we evaluated the effect of cyclic adenosine 3',5' cyclic monophosphate (cAMP) and PGE2 on vasoactive-induced migration of monocytes. RESULTS: Histamine increased (P < 0.003) the migration of monocytes across the filter. This effect of histamine was dose-dependent. Histamine at concentrations of 10(-8) to 10(-5) mol/L induced optimal migration across the filter (control, 16.6 +/- 1.1 vs histamine, 10(-8) mol/L, 40.9 +/- 0.9 monocytes/high power field). Cimetidine, an H2 receptor blocker, attenuated (P < 0.001) the effect of histamine on the migration of monocytes. PGE2 inhibited the migration of monocytes in a dose-dependent manner. Histamine increased (P < 0.001) the passage of monocytes across the glomerular endothelial cell layer (control, 1012 +/- 37 vs 1711 +/- 163 cpm/well). Histamine also increased the migration of murine macrophages across the glomerular endothelial cell layer. PGE2 inhibited the migration of monocytes across the endothelial cell layer under basal as well as histamine-stimulated states. Dibutyryl cyclic (DBc) AMP also attenuated the migration of monocytes under basal as well as histamine-stimulated states. Both PGE2 and DBcAMP also attenuated the IL-1 beta-stimulated migration of monocytes. Angiotensin II, endothelin-1, and platelet-activating factor did not modulate the migration of monocytes. CONCLUSIONS: Vasoactive agents directly modulate the transmigration of monocytes. The present in vitro study provides a basis for a hypothesis that vasoactive agents may also be modulating the migration of monocytes across the glomerular endothelial cell layer (into the mesangium).     

Impaired production of TNF-α by dendritic cells of older adults leads to a lower CD8+ T cell response against influenza

Seasonal influenza causes more morbidity and mortality in older adults than in young adults, apparently because of a decline in immune function with increasing age, known as immunosenescence. In this study, we compared the capacity of dendritic cells (DCs) from healthy older adults (≥65 years) with DCs from healthy young adults (20-40 years) to initiate a T cell response against influenza. DCs from older adults were impaired in the induction of influenza-specific CD8+ T cells as compared to DCs from young adults, which was demonstrated by a decreased proliferation, an impaired production of IFN-γ and a reduced expression of the degranulation marker CD107a by CD8+ T cells. Importantly, DCs from older adults produced significantly less TNF-α, showed a decreased expression of HLA class I and had a lower maturation state after influenza virus infection. Supplementing TNF-α increased the expression of HLA class I and of maturation markers and enhanced the induction of the influenza-specific CD8+ T cell response. Together, these findings indicate that the impaired influenza-specific CD8+ T cell response in older adults is associated with a reduced production of TNF-α and with a lower DC maturation. We suggest that the production of TNF-α is a determining factor in the DC-mediated CD8+ T cell response against influenza.     

Effect of increased glucose load on maternal-fetal transport of alpha-aminoisobutyric acid in the perfused human placenta: in vitro study

The role of hyperglycemia on modulation of maternal-fetanl transport of amino acids in humans is little understood. Hence, we have explored the effect of increased glucose load on transport kinetics of a model non-metabolizable amino acid, alpha-aminoisobutyric acid (AIB), in the human placenta in vitro. Transport kinetics of AIB in maternal-fetal direction was studied using perfusion of isolated human placental lobules. NCTC (National Culture and Tissue Collection)-135 medium, diluted with Earle's buffered salt solution was used as the perfusate and tritiated water was used as the reference marker. Effect of increased glucose load on transport kinetics of study and reference substances was studied in normal term placentae (n=5; gestational age, 38.5±0.5 weeks) in succeeding experimental phases, after a control perfusion phase with physiological glucose concentration. AIB transport fraction (TF), relative to tritiated water TF, averaged 54.8% in control euglycemic phase while in hyperglycemic concentration phases of 27.8 and 55.6 mM, the AIB TF index averaged 42.4% and 38.2%, respectively. Analysis of variance revealed that the difference was statistically significant. Similarly, absorption rate index of the amino acid was also significantly lower in the hyperglycemic perfusion phases compared t control euglycemic phase. We conclude that hyperglycemia may play a deleterious role in limiting maternal-fetal transport of A-type amino acids in the in vivo state. Received: 5 July 2001 / Accepted in revised form: 3 December 2001     

Disseminated coxsackievirus B fulminant myocarditis in an immunocompetent adult: A case report: Case of disseminated coxsackievirus myocarditis

Coxsackieviral myocarditis is associated with systemic involvement in neonates; however, fulminant coxsackieviral myocarditis is rare in adults, and its dissemination with fatal myocarditis involving kidneys, liver, and adrenal is further rarely reported. We report a case of fulminant myocarditis along with dissemination of coxsackievirus, which was clinically unrecognized.     

Chronic Aflatoxin Exposure and Cognitive and Language Development in Young Children of Bangladesh: A Longitudinal Study

Aflatoxin can cross the blood–brain barrier, damage brain tissues, and have the potential to harm the development of the human brain. Although dietary aflatoxin exposure is common in children, there is a paucity of data on aflatoxin exposure and child developmental outcomes. The child’s cognitive, motor, and language functions were assessed using the Bayley Scales of Infant and Toddler Development-III or BSID-III at the same time points. Association between exposure to aflatoxin and subtests of BSID-III were examined using mixed-effect linear regression. Aflatoxin assays were performed on 194, 167, and 163 children at 15, 24, and 36 months of age, and chronic aflatoxin exposure was detected in 20.6%, 16.8%, and 60.7% of children, respectively. Multi-variable analyses showed that aflatoxin exposure was independently related to the children’s cognitive score (β: −0.69; 95% CI: −1.36, −0.02), receptive language score (β: −0.90; 95% CI: −1.62, −0.17), and expressive language score (β: −1.01; 95% CI: −1.96, −0.05). We did not observe any association between exposure to aflatoxin and the motor function of children. Chronic exposure to aflatoxin exposure was linked to reduced cognitive, expressive, and receptive language scores of the study children. Further research is needed in a different setting to confirm this novel finding.