Histopathology of the larval midgut of Helicoverpa armigera (Hübner) fed on Bacillus thuringiensis crystals and Bt-tomato plants.

The histopathological effects of the spore-crystal complex of indigenous Bacillus thuringiensis (Bt) isolate, as well as Cry 2Ab gene expressed in transgenic tomato plants on the midgut of 4th instar larva of Helicoverpa armigera (Hübner) (Lepidoptera: Noctuidea) has been investigated using the transmission electron microscope (TEM). Remarkable ultrastructural changes were observed in the columnar and goblet cells of the larval midgut after feeding on either transgenic tomato leaves, or spore-crystal complex of Bt. The effects observed included breakdown of microvilli of epithelial cells, increase in the electron density of the cytoplasm and vacuolation associated with different sizes of lysosomes; interruption of the goblet cells and distorted goblet cavities which lost their cytoplasmic projections; destruction of the mitochondria which lost their cristae; degeneration of the endoplasmic reticulum; collapse of the nucleus associated with rupture of nuclear envelope and clumped chromatin. Feeding the larvae on transgenic Bt-tomato plants caused in addition to the aforementioned changes severe vacuolation and degeneration of the nucleus in both columnar and goblet cells and the nuclear membrane was broken into electron dense ring spheres.

The hair follicle melanocytes in vitiligo in relation to disease duration.

BACKGROUND AND AIMS: Vitiligo is an acquired pigmentary disorder of skin and hair. Active melanocytes in hair follicles can be detected by DOPA and immunohistochemical staining, while amelanotic melanocytes can only be detected by the latter. None of the studies on hair melanocytes in vitiligo discussed the effect of disease duration on these melanocytes. Here, we study the presence of melanotic and amelanotic melanocytes in vitiligo hair follicles and statistically correlating their presence with the disease duration. METHODS: This study was conducted on 30 patients with vitiligo and 10 normal volunteers. Three biopsies were taken from each patient: two from black and white hairs from vitiliginous areas and the third from apparently normal skin of the same patients. Sections were stained by DOPA reaction and NKI/beteb then examined for the presence of melanocytes. The presence of melanocytes and the disease duration were correlated statistically using the t-test. RESULTS: Active melanocytes were detected in black hairs of 6.7% of vitiligo patients and in 100% of apparently normal skin of the same patients and controls. On examining black hairs of the 28 vitiligo patients with negative DOPA reaction, 19 of them (67.9%) showed positive NKI/beteb stain. Disease duration was inversely correlated with the melanocytes' presence within hair follicles. Melanocytes were absent from 100% of white hairs. CONCLUSIONS: The melanotic melanocytes were the first target of the disease process followed by the amelanotic melanocytes. Since the disappearance of the latter was inversely correlated with the disease duration, early treatment in vitiligo is advised.

Tuberculous pericardial effusion--mediastinal lymph glands: the cause and clue to the etiology.

BACKGROUND: Tuberculous pericardial effusion is most often due to the spread of tuberculosis from the mediastinal lymph glands; however, no attempt has yet been made to study these glands. We studied the mediastinal glands in proven tuberculous pericardial effusion patients and hypothesized that the findings may be of use in the etiological diagnosis of pericardial effusion. METHODS AND RESULTS: We studied 45 patients with large pericardial effusion or tamponade. All underwent chest computed tomographic studies that were reviewed by radiologists blinded to the diagnosis. Of these 45 patients, 27 had tuberculosis and 18 had viral or idiopathic effusion. Pericardial biopsy was done in 25/27 and tuberculin skin test in 22/27 patients with tuberculosis, and all received specific treatment. In patients with tuberculosis the skin test measured 17+/-3.3 mm. All 27 had mediastinal lymph glands > or = 10 mm in size. The mean size of the mediastinal glands was 19.5+/-8.6 mm and the mean number was 2.5+/-1.2. The aortopulmonary glands were the most frequently enlarged (63%), and hilar the least often (14.8%). The glands showed a hypodense center in 52% of the patients. On follow-up of 15.8+/-10.4 months, glands were not seen in 80.9%, and were smaller in size in 19%; none had a hypodense center. Marked lymphadenopathy was not seen in any patient with viral/idiopathic pericardial effusion. Two had glands < or = 5 mm in size. CONCLUSIONS: Only patients with tuberculosis had substantial mediastinal lymph gland enlargement and not those with viral or idiopathic pericardial effusion. Such glands disappeared or regressed on treatment. In the appropriate clinical context, marked nonhilar mediastinal lymphadenopathy on chest computed tomographic studies along with a strongly positive tuberculin skin test could be of value in the noninvasive diagnosis of pericardial effusion due to tuberculosis.