Tubercular cold abscess over the manubrium sterni.
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Abscess↗
Biomedical subjects
M K Bhatnagar
Publications and source records attributed to M K Bhatnagar.
Trauma in the Afghan guerrilla war: effects of lack of access to care.
Little or no acute medical care or evacuation capability was available to resistance forces in the Afghanistan War. We examined the effects of these constraints through a review of 1373 patients admitted to a Pakistani border hospital from 1985 to 1987. Most wounds were to the extremities (92%). Serious complications from injuries were found in 41% of cases, of which the leading causes were soft-tissue infections (36%), chronic osteomyelitis (25%), and marked restriction of joint movement (18%). For 201 patients with known cause of injury, the distribution of responsible weapons was similar to the wars in Korea, Vietnam, and the Falkland Islands. The ratio of critical-area wounds (trunk, head and neck)/extremity wounds was low (0.07) compared with most other wars (about 0.50), indicating that the most seriously injured patients died before treatment was obtained. These early deaths and the many complications from injuries reflect the lack of appropriate surgical attention and evacuation facilities in the field. It is proposed that the ratio of wounds in critical areas to wounds in the extremities might be useful in monitoring the efficiency of evacuation in similar conflicts. Early surgical management and evacuation of battle casualties could have greatly reduced mortality from the war and subsequent disabilities.
Adolescent↗
Ultrastructure of kidney of ducks exposed to methylmercury, lead and cadmium in combination.
Ultrastructural alterations in the kidneys of Pekin ducks exposed to various combinations of methylmercury chloride (MeHgCl), lead acetate (PbAC) and cadmium chloride (CdCl2 for 12 weeks were studied. Eight groups (Gr), each consisting of 6 female ducks, were fed diets containing no heavy metals (control), 8 mg of methylmercury chloride (MeHgCl)/kg of feed (GrII), 80 mg of lead acetate (PbAC)/kg of feed (GrIII), 80 mg of cadmium chloride (CdCl2)/kg of feed (GrIV), 8 mg of MeHgCl + 80 mg of PbAC/kg of feed (GrV), 8 mg of MeHgCl + 80 mg of CdCl2/kg of feed (GrVI), 80 mg of PbAC + 80 mg of CdCl2/kg of feed (GrVII), and 8 mg of MeHgCl + 80 mg of PbAC + 80 mg of CdCl2/kg of feed (GrVIII). Renal corpuscles of the ducks treated with methylmercury (MdHg), lead (Pb), the cadmium (Cd), either alone or in two way combinations exhibited minor ultrastructural changes. The thickness of the glomerular basement membrane was significantly different from control only in Grs II, IV, V and VI. Crystallization of granules in the juxtaglomerular cells was also observed in Cd and Pb treated birds. Administration of the three metals in combination caused marked changes in podocytes with fusion of secondary processes and no pedicle differentiation. The proximal tubule cells approximately (PT) accumulated lipid droplets, lysosomal bodies and membrane bound vacuoles in methylmercury treated birds. Lead exposed birds had a large number of secondary lysosomes and swollen mitochondria in PT cells. Cadmium administration caused degenerative changes in PT cells which included accumulation of lysosomal bodies containing degenerating organelles, lipid droplets and vacuoles containing myelin figures. Marked degenerative changes in PT cells and interstitial fibrosis was prominent when cadmium was concomitantly administered with the other metals. Concurrent administration of all three metals caused enhancement of degenerative changes in proximal tubule cells and collecting duct cells. These observations suggest that the combined administration of metals causes renal damage that appears to be additive.
Animals↗
Combined toxicity of ethanol and methylmercury in rat.
The hepatotoxic and nephrotoxic effects of methylmercury (CH3Hg) and ethanol (EtOH) are well known; however, their interaction in vivo is not clearly understood. In order to investigate the combined effects of these 2 substances, 4 groups of male Wistar rats with an initial weight of approximately 190 g were treated for 7 weeks. Each group consisting of 8 rats was gavaged as follows: Group 1 with 5.0 ml/kg body weight of double distilled water, Group 2 with 5.0 ml/kg body weight of 25% EtOH, Group 3 with 2.5 mg/kg of CH3Hg in water, and Group 4 with 2.5 mg/kg of CH3Hg in 25% EtOH. At the termination of the experiment the mean body weights of the rats in Group 3 (372.5 +/- 10.8 S.E.) and Group 4 (383.4 +/- 13.4) were significantly lower than that of Group 1 (433.0 +/- 7.8). Linear regression showed a positive feed conversion efficiency for Groups 1 and 2 (1.07 and 0.83, respectively), and a negative score for this parameter for Groups 3 and 4 (-1.43, -1.53). At necropsy, rat livers from Group 3 exhibited random multifocal tan spots. The relative liver weights were similar to those of controls. Semithin sections of liver revealed an increase in lipid droplets in Groups 2 and 3 compared to those in the other 2 groups while vacuolization was more striking in CH3Hg treated rats (Groups 3 and 4). Severe hepatolysis and portal canal edema were noted in the groups of rats exposed to either EtOH alone or in combination with mercury. The relative weight of left kidney in Group 3 (0.70 +/- 0.03) and Group 4 (0.51 +/- 0.04) rats was significantly greater than that of the control (0.39 +/- 0.03). In gross appearance the kidney was pale and the urine production was significantly higher (P less than 0.05) in Group 3 compared to that of Group 1. Group 4 rats had significantly more (P less than 0.05) Hg in the kidney than Group 3; however, the inorganic percentages in both groups were similar. Morphological examination of the kidney proximal tubules from CH3Hg treated rats (Groups 3 and 4) revealed an increase in lipid droplets, vacuoles, cell sloughing and tubular degeneration compared to Groups 1 and 2. These histological changes in the proximal tubules of Group 4 rats indicate an additive effect of EtOH on the kidney pathology caused by CH3Hg.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Ultrastructural alterations in the kidneys of Pekin ducks fed methylmercury.
Ultrastructural alterations in the kidneys of Pekin ducks were studied after subchronic exposure to methylmercury chloride. Twenty-four male and twenty-four female Pekin ducks, 12 weeks of age were fed 0.0 (control), 0.5, 5.0 and 15.0 parts per million of MeHgCl, mixed in a mash diet for 12 weeks. Birds were observed for clinical signs daily. Kidneys were fixed in situ by perfusion with 4% glutaraldehyde in 0.05 M phosphate buffer and routinely processed for electron microscopy. Only minor morphological changes were observed in the renal corpuscle of ducks in the 0.5 ppm group. The component cells of the renal corpuscle in the 5.0 and 15.0 ppm groups showed several ultrastructural alterations, including an increase in number and size of lysosomes and vacuoles in podocytes and mild vacuolation in mesangial cells. The juxtaglomerular cells of afferent arterioles had crystallized granules. No significant changes were observed in glomerular basement membrane thickness and width of podocyte pedicels. The proximal tubules of the 5.0 and 15.0 ppm groups showed some microvillar loss and an increase in the number and size of lipid droplets, vacuoles and lysosomal bodies. The distal tubular changes in the 5.0 and 15 ppm groups included electron lucency and vacuolation of cytoplasm as well as occasional mitochondrial swelling. The collecting ducts of 5.0 ppm and 15.0 ppm groups showed varying degrees of degenerative changes in both mucus secretory as well as absorptive cells. These results suggest that subchronic exposure of Pekin ducks to methylmercury chloride causes subtle ultrastructural changes in renal corpuscle and marked ultrastructural changes in proximal tubules and collecting ducts.
Animals↗
Scanning and transmission electron microscopic studies on the oviducts of Pekin ducks fed methyl mercury containing diets.
This study was undertaken to examine the effects of varying levels of methyl mercury (MeHg) on the ultrastructure of the surface epithelium of the oviduct of ducks. Accordingly, Pekin ducks were maintained on feed containing varying doses of (0.0; 0.5; 5.0; 15.0 ppm) of MeHg (Group I - control to IV) for 12 weeks and sacrificed. Tissue from the magnum and the shell gland regions of the oviduct was processed for scanning electron microscopy (SEM) and transmission electron microscopy (TEM). It was found that the primary and secondary folds of these regions of the oviducts of the control and 0.5 ppm treatment group were densely populated with ciliated cells and that the cilia tend to cover the apical surfaces of the non-ciliated secretory cells. This unchanged ultrastructural morphology of the surface epithelium of 0.5 ppm treatment group was verified with TEM. The ciliated and nonciliated cells in surface epithelium appeared to be equal in frequency. The nuclei of ciliated cells were superficial in location compared to nonciliated secretory cells which had nuclei in the basal part of the cytoplasm. In the oviductal tissues from ducks fed 5.0 ppm MeHg isolated areas of ciliary loss, but minimal disruption of the apical plasma membrane were observed by SEM. In a few birds plasma membrane lesions, condensation of nuclear chromatin and very dilated rough endoplasmic reticulum were seen with TEM. In the oviductal tissues from ducks fed 15.0 ppm MeHg it could be seen that ciliary loss was much more extensive than hitherto observed, and disruption of the apex of cells could be seen. TEM showed degeneration of cytoplasmic organelles, more or less severely damaged ciliated cells, loss of ciliary extensions and formation of compound cilia. These observations indicate that methyl mercury at 5.0 and 15.0 ppm dose levels causes toxic injury to oviductal surface epithelium of Pekin duck that may cause reduced reproductive capability.
Animals↗
Ultrastructure of the testis of Pekin ducks fed methyl mercury chloride: seminiferous epithelium.
Testicular cells of Pekin ducks (Anas platyrhynchos) fed with 0 (control), 0.5 (group 1), 5 (group 2), or 15 (group 3) mg of methyl mercury chloride (CH3HgCl)/kg of basal feed for 12 weeks were examined by electron microscope. Sertoli's cells from ducks in group 2 had dilated smooth endoplasm reticulum, increased lysosomes, and large vacuoles, some with lipid droplets. Degenerative changes were more advanced in group 3 ducks. There were increases in lysosomes, myelinoid figures, vacuolations, cytoplasmic and nuclear debris, cristolyses of mitochondria, and distended Golgi's complexes, and a reduction in smooth endoplasm reticulum and microtubules when compared with those of the controls. Spermatogonia were resistant to CH3HgCl exposure, except in 2 ducks from group 3 which had cells that showed electron-lucent cytoplasm, abnormal mitochondria, and membrane-bound vacuoles. In primary spermatocytes, degenerative changes were evident in ducks fed the larger dose levels. In nuclei, synaptonemal complexes showed unpaired elements. In cytoplasm, cellular debris and vacuoles predominated. There was an increase in synchronized meiosis and apparent incomplete cell division. In ducks from group 3, the cellular damage was more severe and was present throughout the germinal epithelium. Spermatids differentiation was affected variably in groups 2 and 3. Severity of damage increased with the increased dosage of mercury. Where there was spermiogenic activity, the electron-dense acrosome granules, manchette, and midpiece were rarely found. Since the seminiferous tubules from 2 ducks in group 3 had severe destruction of spermatocytes and spermatids, the spermiogenic activity was negligible. Ingestion of CH3HgCl caused toxic injury to seminiferous tubules in groups 2 and 3 ducks. The degree of damage was related to the dietary amount of mercury.
Administration, Oral↗
Ultrastructure of turkey hepatocytes.
Hepatocytes of normal male and female turkey livers perfused in situ with a fixative containing 4% glutaraldehyde in 0.05 M phosphate buffer (pH 7.4) were examined by electron microscopy. The hepatocytes, arranged in two-cell-layered plates, were polygonal and had three spatially different surfaces. The vascular surface was formed by microvilli, which at times projected into the sinusoids past the space of Disse. The interhepatocytic surfaces were closely applied and contained an occasional gap junction. The biliary surface participated in bile canaliculus formation and had short, regular microvilli. Tight junctions and adherens junctions were close to the canalicular lumen. The hepatocyte nucleus was located towards the vascular pole. The cytoplasm of hepatocytes of the females had many lipid droplets. The pleomorphic mitochondria, with relatively electron dense matrices were surrounded by one or, rarely, two profiles of flattened rER. Golgi complex was often observed in the vicinity of the nucleus, whereas the centrioles were located in the pericanalicular area of the biliary pole, which was rich in microtubules. These microtubules were extremely long, at times covering a substantial distance between the Golgi complex and bile canaliculi; microtubules occasionally formed bundles near the biliary pole. Small vesicles in close proximity of the microtubules were frequently observed. The spatial relationship between Golgi complex, microtubules, vesicles, and centrioles at the biliary pole of the hepatocyte appears to support the concept that the bile secretory mechanism in avian hepatocytes may involve a centrioles-microtubules-vesicles-Golgi complex system.
Animals↗
Ultrastructure of the thyroid glands of rats fed photomirex: an 18-month recovery study.
The thyroid glands, from rats which had received photomirex (0.05, 0.5, 5 or 50 ppm) or mirex (5 or 50 ppm) in their diets for 28 days and maintained for 18 months on clean diet, were examined by electron microscopy. A dose of 0.05-5 ppm photomirex resulted in an augmentation of principal follicular cell heights. Their cytoplasm exhibited a marked numerical increase of secondary lysosomes. In addition, at 5 ppm, follicular cells in some segments of the gland contained only a few secondary lysosomes. After dietary exposure to 50 ppm photomirex the number of lysosomal elements remained elevated in epithelial cell cytoplasm. Morphological aberrations in the follicles could not be detected after the 5 ppm mirex treatment. The most remarkable alterations in this experiment occurred in the thyroid glands of animals ingesting 50 ppm mirex where columnar follicular cells were engorged with deformed lysosomal bodies. Remaining components of the follicular cell architecture in all the treated groups were unaffected and were similar to those in the control group. These results demonstrated that following a 28-day dietary exposure of rats to photomirex (0.05-50 ppm) or mirex (50 ppm), alterations in the thyroid glands persisted for at least 18 months.
Administration, Oral↗
Ultrastructural alterations of the liver of Pekin ducks fed methyl mercury-containing diets.
This report describes the ultrastructural alterations of the liver of 24 male and 24 female Pekin ducks fed 0.0, 0.5, 5.0, and 15.0 ppm of methyl mercury chloride (MeHgCl), mixed in a mash diet, for 12 wk. Birds were weighed weekly and observed for neurologic symptoms daily. Samples of blood, liver, kidney, skeletal muscle and brain were analyzed for Hg residue by atomic absorption spectrophotometry. Livers were fixed in situ by perfusion with glutaraldehyde fixative and processed for electron microscopy. The percent decreases in mean body weights between wk 0 and wk 7 were statistically not significant except for males fed 5.0 ppm MeHgCl. Leg paralysis and convulsions in males treated with 15.0 ppm began at wk 5 and in females at wk 8, but were more severe in the latter. The dose-residue response for the three dose levels in all five tissues was linear, with liver and kidney containing the highest and the brain the least amount of Hg. Hepatocytes in 0.5- and 5.0-ppm MeHgCl treatment groups showed little morphologic changes, while liver cells in the 15.0-ppm group had several ultrastructural alterations, including remarkable increase in peribiliary lysosomal bodies. The mitochondria of some hepatocytes exhibited lysis of both inner and outer membranes. Changes also occurred in endothelial and Kupffer cells. These results indicate that dosing Pekin ducks with 15.0 ppm causes ultrastructural alterations indicative of toxic injury to the liver.
Animals↗
Ultrastructural study of liver fibrosis in turkeys fed diets containing rapeseed meal.
Livers of turkeys fed low and high glucosinolate rapeseed meal diets for 16 weeks were examined ultrastructurally. Hepatocytes from birds fed on Tower rapeseed meal (0.15 mg of glucosinolate per g) showed a mild accumulation of lipid droplets and an apparent increase in lysosomes and microbodies. The parenchymal cells of the livers of turkeys fed on Target Rapeseed meal (9.50 mg of glucosinolate per g) exhibited varying degrees of degenerative change: dilation of endoplasmic reticulum, swelling of mitochondria with fragmentation and loss of cristae, presence of autophagic vacuoles, myelinoid bodies, electron-dense lipidlike droplets, vesiculation of cytoplasm and necrosis of the hepatocytes. The electron-dense lipidlike bodies were most frequent at the biliary pole. Sinusoids near the degenerating hepatocytes were often disrupted and perisinusoidal mesenchymal cells in the area showed distended cisternae of granular endoplasmic reticulum. Such cells or fat-storing cells were frequently seen in the vicinity of proliferated collagen fibrils and degenerating hepatocytes. These observations suggest that degenerative alterations of hepatocytes accompanied or preceded the development of fibrosis in turkeys fed rapeseed meal high in glucosinolate.
Animal Feed↗
Ultrastructural alterations of the myocardium of rats fed rapeseed oils.
Ultrastructural studies were conducted on the myocardium of rats fed corn oil, Tower RSO (0 . 88 per cent EA), 1788 RSO (3 . 6 per cent EA) and Target RSO (38 . 9 per cent EA) supplemented diets for 18 weeks. Cardiac myocytes of Tower RSO-fed rats showed some loosening of myofibrils and a slight increase in the number of mitochondria, few of which had lost their cristae. Large intravascular lipid droplets were observed in the myocardium of rats fed the 1788 RSO diet, as well as some small lipid droplets which were seen in close association with mitochondria. There was an apparent increase in the number of mitochondria of both normal and giant size. Many of the mitochondria exhibited distortion of shape and degeneration of cristae. The matrix of megamitochondria contained vesicles and electron-dense floccular inclusions and at times electron-lucent lipid-like material. The degenerative changes of mitochondria were most pronounced in the Target RSO group, where some megamitochondria showed a complete loss of cristae and a replacement of matrix with lipid-like material. These observations suggest that both intravascular lipid globules and the mitochondrial alterations are possible contributory factors involved in the development of cardiac lesions in RSO-fed rats.
Animals↗
Microbodies of the pig liver. A morphologic and morphometric study.
The ultrastructure of hepatic microbodies of pigs was studied in liver samples fixed in phosphate-buffered 2% glutaraldehyde (pH 7.4) and postfixed in 2% osmium tetroxide. The microbodies were rounded or ovoid in shape and contained a granular matrix enclosed with a single limiting membrane. The matrix, in many of the organelles, contained an amorphous or an organized (crystalloid) area. The crystalloids were organized as fine, alternating electron-opaque and electron-lucent lines, or as groups of tubules arranged in more than one plane. Profiles of smooth endoplasmic reticulum were usually found near the microbodies. 34 microbodies were approximately 0.67 +/- 0.02 micrometer (mean +/- standard error) in length and were approximately 0.56 micrometer (+/- 0.02 micrometer) wide. The marginal plates consisted of strata which exhibited a periodicity. The average length and width of 17 plates was approximately 0.34 +/- 0.03 micrometer and 0.002 micrometer, respectively. This study clearly establishes the occurrence of marginal plates in microbodies of porcine liver.
Animals↗
Histopathology of the heart from rats fed rapeseed oils.
The cardiopathogenicity of oils from new, low erucic acid (EA) rapeseed, Brassica napus, cv Tower (0.88 per cent EA) and Brassica napus, cv 1788 (3.6 per cent EA) were tested on rats following 18 weeks of feeding. Oil from Brassica napus, cv Target, with 38.9 per cent EA served as a positive control and corn oil as the negative control. Tower and 1788 rapeseed oils showed noticeable cardiopathogenicity, and a few mild lesions were also noted in the corn oil group. The main pathological change was from fresh to relatively old foci of myocardial necrosis. The presence of droplets accompanying the platelet aggregates suggested the possibility of their involvement in the development of the lesions. The pathological changes in the small and minute blood vessel walls were interpreted as one of the predisposing factors for the development of fatty embolism and subsequently of myocardial necrosis.
Animals↗
Histochemical localization of 3 beta-hydroxysteroid dehydrogenase in the testes of chicken-pheasant hybrids.
Histochemical studies on the activity of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) in the testes of adult chicken-pheasant hybrids and domestic fowl of similar age were carried out using dehydroepiandrosterone as the substrate. The reaction for 3beta-HSD was positive in the interstitial tissue and negative within seminiferous tubules of domestic fowl. In chicken-pheasant hybrids, a strong positive reaction for 3 beta-HSD was observed in the interstital tissue and within the seminferous tubules suggesting that, in hybrid testes, both Leydig cells and cells of seminiferous tubules may be capable of steroid biosynthesis. Since the plasma testosterone levels in these birds were found to be extremely low, it is hypothesized that either the chicken-pheasant hybrids do not release testosterone in sufficient amounts in the circulation or the type of steroid produced by the 3 beta HSD-positive cells may be different from testosterone that is required for the maintenance of normal fertility and the development of secondary sexual characteristics.
Animals↗
Intravascular fat globules in the heart of pigs fed rapeseed meals.
Histopathological studies were conducted on growing pigs fed a corn, soybean meal control and two experimental diets supplemented with either a high or a low glucosinolate rapeseed meal. A high incidence of intravascular large fat globules in the heart with mild interstitial oedema was observed in the boars on high glucosinolates in comparison with the boars on low glucosinolates rapeseed meal. Boars and gilts on the corn, soybean meal control diet showed no intravascular fat globules.
Animal Feed↗
Liver fibrosis of the turkey on rapeseed products.
Sclerosis of the liver accompanied by hydropericardium of long standing was observed in turkeys fed rapeseed products for 16 weeks. Histologically, extensive increases of fibrous tissue composed predominantly of reticular fibres and centrilobular degeneration of parenchymal cells were the main pathological features. Neither prominent fatty degeneration nor the formation of pseudolobules was observed. The birds fed rapeseed products for four and 12 weeks showed continuing occurrence of multiple focal and/or solitary hepatocytic necroses preceding the process of fibrosis in the livers. Glucosinolates and their hydrolytic products were considered the most likely causative factors for the hepatocytic necrosis.
Animal Feed↗
Haemorrhagic liver syndrome of broiler chickens fed diets containing rapeseed products.
Haemorrhagic livers were observed in male white rock chicks of one to four weeks old, that were fed diets supplemented with 50 per cent rapeseed meal and 50 per cent rapeseed full-fat seeds. The haemorrhagic lesions were comparable to those of the laying hens except for the absence of fatty degeneration. There were no substantial fibrotic lesions. Multifocal or solitary hepatocytic necrosis was observed around the haemorrhagic lesions, although the necrotic foci did not always accompany the haemorrhage. The reticulum only of the necrotic and haemorrhagic lesions was not demonstrated with silver strain. Association of hepatocytic necrosis with liver haemorrhage and absence of argyrophilic fibres suggested that the hepatocytic necrosis was the primary contributory factor for the development of the hepatic haemorrhage.
Animal Feed↗