Inoculation of a cultured autologous epidermal suspension containing melanocytes in vitiligo.
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Biomedical subjects
Publications and source records attributed to A K Gulati.
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The present study analyzes the regeneration of skeletal muscle in diabetic rats. Intravenous injection of streptozotocin (STZ) was used to induce diabetes. Six weeks later the extensor digitorum longus (EDL) muscles from diabetic rats were either transplanted into diabetic or normal hosts to initiate regeneration. Normal EDL muscle transplants in normal and diabetic hosts were also performed for comparison. One, 2, 4, and 12 weeks after transplantation, the EDL regenerates were morphologically analyzed. Regeneration and formation of neuromuscular junctions were observed in all transplants, including diabetic regenerates in diabetic hosts. The overall mass and myofiber size of the diabetic EDL regenerate in the diabetic host was significantly reduced in spite of complete regeneration. Recovery of the diabetic muscle mass and the myofiber size was observed after transplantation into normal hosts. A reduction in mass and myofiber size was observed in normal EDL muscles transplanted into diabetic hosts. It is concluded that poor recovery of diabetic muscle is related to metabolic and structural alterations in the diabetic host, rather than to innate capacity of the muscle to per se undergo regeneration and reinnervation. The observed enhancement in recovery of diabetic muscle after transplantation in a normal host and deterioration of normal muscle after transplantation in a diabetic host shows that the host environment determines the success of muscle regeneration.
Glycoconjugates of the extracellular matrix are important for the normal mechanical functions of connective tissue structures such as the temporomandibular joint disc. Since lectins are known to bind to sugar residues with high affinity, a variety of lectins were used to study the presence and distribution of glycoconjugates in the temporomandibular joint disc. Discs were removed from 6 to 8-month-old rabbits and either sectioned in a cryostat and processed for light microscopy or fixed in 2% glutaraldehyde and processed for electron microscopy. The frozen sections were incubated with fluorescein- or peroxidase-conjugated lectin solutions. Ultrathin sections mounted on grids were incubated with lectins combined with a colloidal gold marker system for electron microscopical study. Our results indicate that Canavalia ensiformis agglutinin (ConA) showed little or no binding to the discal tissue. Triticum vulgaris agglutinin (WGA) and Maclura pomifera (MPA) were bound strongly to both the synovium and the extracellular matrix and WGA also bound to the territorial matrix of chondrocyte-like cells. Glycine max and Arachis hypogoea agglutinins (SBA and PNA), were localized in the synovium and extracellular matrix but to a lesser degree than WGA and MPA. WGA, MPA, Griffonia simplicifolia II and Ulex europaeus were bound by discal fibroblasts. WGA was also localized in lysosomes of synovial A-cells (macrophages). The electron microscopical studies with lectins and colloidal gold marker systems indicated that some areas of the disc may be fibrocartilagenous as had been suggested by earlier immunohistochemical studies using monoclonal antibodies to characteristic glycosaminoglycans (GAGs) in cartilage.
Peripheral nerve grafts promote vigorous regeneration of adult mammalian CNS axons. Elimination of nerve-associated cells by freeze-thawing abolishes this promoting quality, possibly by creating inhibitory cellular debris and/or destroying the production of stimulatory factors by living Schwann or other cells. Here, debris-free acellular peripheral nerve segments placed between the disconnected septum and the hippocampal formation acquired almost no cholinergic axons after 1 month. However, such acellular nerve grafts treated before implantation with purified beta-nerve growth factor (NGF) contained nearly as many longitudinally oriented cholinergic axons as did fresh cellular nerve grafts. These results suggest that (i) NGF is required for the regeneration of adult CNS cholinergic axons into nerve grafts and (ii) an important function of living cells within peripheral nerve may be the production of neuronotrophic factors such as NGF.
Acellular basal lamina grafts have recently been reported to support axonal regeneration and have been used in peripheral nerve repair. The present study was designed to determine the immunogenicity of such basal lamina allografts (grafts that are genetically different) and their potential as bridging material for nerve gap repair. Inbred strains of Fischer and Buffalo rats with known histocompatibility differences were used. Acellular grafts were prepared by repeated freezing and thawing nerve tissue predegenerated in situ for 6 weeks. Non-frozen predegenerated nerves were used as cellular grafts for comparison. Fischer rats were used as hosts and received cellular or acellular grafts obtained from Fischer (isograft, genetically identical) or Buffalo (allograft) donors. The grafts were evaluated morphologically at 1, 2, 4, and 12 weeks after transplantation. The cellular isografts supported axonal regeneration best. The cellular allografts were invariably rejected and were unsuccessful or only partially successful in supporting regeneration. In contrast, acellular allografts, in spite of their mild immunogenicity were successful in supporting regeneration, as were the acellular isografts. The rate of host axonal regeneration and recovery of target muscle was reduced in acellular allografts and isografts as compared to cellular isografts. It is concluded that acellular allografts are suitable for supporting axonal regeneration and may be used to bridge gaps in injured peripheral nerves.
One hundred patients of vaginitis along with 50 age matched control women were studied. Non-specific vaginitis (NSV) was diagnosed on the basis of the presence of at least any three of the four parameters which included presence of thin gray homogeneous discharge, pH of the discharge greater than or equal to 4.5, liberation of fishy odour from the discharge after adding 10 per cent KOH and presence of clue cells Using these criteria, NSV was diagnosed in 22 of the 100 patients and in 4 of 50 control women. Gardnerella vaginalis was cultured from 23 of the 26 women with NSV and 19 women without NSV (8 patients and 11 normal women). Women with NSV showed statistically significant difference in the presence of clue cells, amine test positivity and concentration of G. vaginalis as compared to women without NSV.
Cord blood samples collected from 150 newborns were tested for HBsAg using micro ELISA technique. Only 8 (5.3 per cent) out of 150 samples were found to be positive for HBsAg in variable titres. It is important to identify these HBsAg positive newborns so that appropriate measures could be adopted at the earliest to prevent the complications of HBsAg carriage.
Antibodies specific for fibronectin were utilized to determine the sites of localization in the liver during development. The livers of fetal rats from each of gestation days 11-19, and from days 1 and 8 postpartum, were studied by fluorescence microscopy. Fibronectin was localized predominantly in megakaryocytes and megakaryocyte precursors, and to a lesser extent in the extracellular matrix surrounding blood vessels and between hepatocytes and sinusoids. The cytoplasm of megakaryocytes and their precursors displayed bright fluorescence but their nuclei were negative for fibronectin. Hepatocytes had negative or faint fluorescence. Megakaryocytes were present in the liver from day 12, and were numerous from day 13 through most of the rest of gestation. The relative numbers of megakaryocytes decreased in later gestation; at 8 days postpartum only a few were observed per section. Hepatic megakaryocytes appeared before megakaryocytes were established in spleen and bone marrow. The early and persistent high levels of fibronectin in hepatic megakaryocytes, in the absence of comparable localization within hepatocytes, leads us to the hypothesis that megakaryocytes are important in establishing circulating fibronectin levels in the fetus. Similarly, bone marrow megakaryocytes may contribute to circulating fibronectin in the adult.
The present study describes the usefulness of blood vessel allografts to repair gaps in rat peripheral nerve after immunosuppression with cyclosporine. Isogeneic strains of rats with known histoincompatibility were used for this study. A 10-mm gap was created in the peroneal nerve of host Fischer rats. The gap was bridged by a 12-mm section of internal carotid artery removed from a Buffalo strain of rat. The host rats were divided into two groups. One group received no immunosuppression, whereas the other group was treated with cyclosporine. Untreated control rats immunologically rejected the allografted vessels and were unable to support host axonal regeneration through them. On the other hand, in cyclosporine-treated rats the allografted vessels survived. The regenerating host axons reorganized to form a functional nerve within the vessel conduit. The regenerated axons persisted even after rejection of the allografted vessel caused by cessation of immunotherapy. These results show that blood vessel allografts can serve as an effective conduit for reorganization of regenerated nerves and can bridge gaps in peripheral nerves.
A total of 100 women with vaginitis and 50 age matched healthy women were studied for common infective agents of vaginitis. The vaginal secretions collected from these women were examined for Trichomonas vaginalis, G. vaginalis, and Candida species. The prevalence of infective agents in the patients was T. vaginalis 11 per cent. Candida species 30 per cent and Gardnerella vaginalis 31 per cent. In contrast, in the control group the prevalence was Candida species 14 per cent and G. vaginalis 22 per cent. T. vaginalis was not isolated from any of the control women. Mixed infections with G. vaginalis and Candida species were seen in four cases and T. vaginalis and Candida species in one case only. Mixed infection with T. vaginalis ahd G. vaginalis was not observed in any of the patients studied.
Twenty patients with aphthous ulcers were advised deglycyrrhizinated liquorice (DGL) mouth wash and were followed for two weeks. Fifteen patients experienced 50-75% improvement within one day followed by complete healing of the ulcers by third day.
We have presented a case of a 28-year-old woman with an intrasacral meningocele. Diagnosis of this case was aided by the use of MRI. The literature regarding this problem has been reviewed.
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The present study examines the influence of denervation on the regenerative ability of skeletal muscle in rats. Muscle denervation was achieved by transecting and ligating the cut ends of the sciatic nerve. Four to 48 weeks after denervation, the extensor digitorum longus (EDL) muscle was autotransplanted to induce muscle regeneration. The transplanted EDL muscles were examined at 1-12 weeks. Normal (i.e., no prior denervation) EDL muscle autotransplants were also examined for comparison. Denervation resulted in progressive atrophy of muscle, marked by a reduction in the size of myofibers and an increase in endomysialperimysial connective tissue. In spite of these alterations, typical events of muscle regeneration were invariably observed after transplantation. Initial myofiber degeneration and subsequent regeneration of myotubes occurred in a manner similar to normal muscle transplants. However, only a partial maturation of myotubes was observed in denervated muscles. These results show that extended denervation does not abolish the capability for muscle regeneration. The precursor myosatellite cells, proposed to be responsible for muscle regeneration, retain their regenerative potential after denervation. It is concluded, however, that the presence of intact innervation is crucial for the terminal differentiation and maturation of regenerating muscle.
We studied the fate of skeletal muscle obtained from patients with amyotrophic lateral sclerosis (ALS) after transplantation into immunodeficient nude mice. The transplanted muscle consistently survived in the nude mice without immunological rejection. The myofibers in these muscles underwent degeneration, followed by regeneration, maturation, and eventual functional innervation by the mouse motor neurons. The ability to grow diseased human muscle successfully over a prolonged period in nude mice offers an in vivo model to study the etiology of ALS and possibly of other neuromuscular disorders.
Nerve grafts composed of basal lamina scaffolds and lacking viable Schwann cells have recently been shown to be effective in supporting axonal regeneration. As only short grafts were used in those studies, the present investigation was conducted to evaluate the ability of long acellular basal lamina nerve grafts and equivalent cellular grafts to support axonal regeneration for nerve gap repair. Cellular grafts consisted of nerve segments that had degenerated in situ for 4 weeks. Acellular grafting material consisted of similar segments that were repeatedly frozen and thawed to kill all cells prior to grafting. The results show that host axons can regenerate through the entire 4-cm length of cellular grafts but not through acellular basal lamina grafts. However, in the acellular grafts numerous axons were seen in the proximal 2-cm region. It is concluded that basal lamina grafts possess limited ability to support axonal regeneration. As in cellular grafts, viable Schwann cells appear to be important for regeneration to occur over longer distances.
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