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Biomedical subjects

T W Huang

Publications and source records attributed to T W Huang.

At least 37 records · Page 2Linked to original sources
PubMed1988

Experimental Escherichia coli epididymitis in rabbits.

We describe an experimental model of bacterial epididymitis in New Zealand white rabbits. Inoculation of 10(7) colony-forming units of Escherichia coli in a retrograde fashion into the vas deferens reliably produced clinical, bacteriologic, and pathologic epididymitis. Inflammation was maximum at two weeks and subsided by one month without treatment. E. coli could be reisolated from the epididymides for up to two weeks post inoculation. We detected loss of spermatogenesis in both the ipsilateral and contralateral testes and the appearance of antisperm antibodies subsequent to the infection in some animals. There were 2 cases (11%) of histologic bilateral epididymitis after unilateral inoculation; one of these had bilateral clinical epididymitis with E. coli recovered from both epididymides at two weeks.

Animals↗
PubMed1988

Reoperative carotid surgery.

Fourteen patients underwent carotid reoperation for symptomatic recurrent carotid stenosis after previous ipsilateral carotid endarterectomy. Eight of these patients presented with focal transient ischemic attacks, two with strokes, and four with vertebrobasilar insufficiency. Recurrent symptoms in eight patients were similar to those prompting the initial carotid endarterectomy. Symptoms recurred early after previous carotid endarterectomy in 2 patients and late in 12 patients. Eleven patients underwent repeat endarterectomy and carotid patch angioplasty, two patients underwent patch angioplasty alone, and one patient underwent carotid artery replacement with a vein graft. Persistent or recurrent focal symptoms referable to the reoperated carotid artery were not present during follow-up (mean 27.4 months, range 4 to 79 months). Vertebrobasilar symptoms were relieved by carotid reoperation in each patient. Although the natural history of asymptomatic postoperative carotid restenosis is unknown, reluctance to reoperate on symptomatic patients is unwarranted, since carotid reoperation can be performed safely with the expectation that recurrent focal and nonfocal vertebrobasilar symptoms will be relieved.

Aged↗
PubMed1985

Podoendin. A new cell surface protein of the podocyte and endothelium.

A new cell surface protein, podoendin, has been identified in Sprague-Dawley rats, and isolated using monoclonal antibody (mAb) G4. The distribution of podoendin is restricted to the surface of glomerular podocytes, urinary surface of the parietal epithelium of Bowman's capsule, and the luminal surface of endothelial cells. The antibody does not crossreact with podocytes or endothelia of human or mice. In newborn rats, the appearance of podoendin on glomerular epithelium is attendant on podocyte differentiation during glomerulogenesis of metanephrogenic vesicles. It disappears when podocytes retract and efface foot processes in tissue culture. Thus, podoendin appears to be a cell differentiation-dependent surface protein of podocytes. Podoendin is a protein of 62 kD mobility on 5% polyacrylamide gel electrophoresis. It stains intensely with Coomassie blue, but gives negative reactions to carbohydrate (periodic acid/Schiff reaction) and polyanions (alcian blue, colloidal iron, and carbocyanine). It is distinct from the major sialoglycoprotein of podocyte fuzzy coat, podocalyxin (11). Podoendin isolated and purified from endothelium of lungs appears to be identical with that from podocytes and endothelium of kidneys. Injection of mAb G4 into left ventricle of rats resulted in intense decoration of the endothelium and podocyte surface within 30 min. The decoration persisted throughout the 3-d period of observation. This was not accompanied by complement (C3) fixation. Preliminary results showed that the rats developed moderate proteinuria (100 mg/ml protein in urine), which was associated with the presence of hyaline droplets in renal tubules, on the third day. The proteinuria was not accompanied by effacement of podocyte pedicels. There were no morphologic alterations indicating glomerular or vascular injury in the kidneys.

Animals↗
PubMed1985

Carcinosarcoma of the floor of mouth.

Carcinosarcomas are rare tumors of the upper aerodigestive tract, consisting of both carcinomatous and sarcomatous tissue. The larynx and oral cavity are most frequently involved. There has been much controversy regarding the histological nature and clinical course of these tumors. We report a case of carcinosarcoma of the floor of mouth in a 76 year old man who presented with a large pedunculated sublingual mass. There was no evidence of regional or systemic metastatic disease. After local excision, he was followed for one year without evidence of recurrence or metastasis. A review of the literature is presented, with an attempt to clarify clinically relevant aspects of nomenclature, pathogenesis, and clinical course.

Aged↗
PubMed1983

Immunohistochemistry of two glycolipid tissue antigens in human gastric carcinoma.

Immunohistochemical studies of two glycolipid tissue antigens were carried out to ascertain their distribution in normal as well as cancerous gastric mucosa. A trihexose ceramide (Kiyo antigen), a precursor of ABH blood group substances, is present in epithelial cell membrane and mucin of 90% (45 of 50) of noncancerous gastric mucosa. The distribution is similar to blood group substance; 10.7% (3 of 28) of gastric carcinoma that arose in Kiyo-positive gastric mucosa exhibited complete loss of the antigen, while carcinomas from Kiyo-negative gastric mucosa remained Kiyo negative. A fucopentaose ceramide (Lex), however, is absent from noncancerous gastric mucosa but present in varying quantity in 92.9% (52 of 56) of gastric carcinomas. The emergence of Lex as a tumor cell marker in the great majority of gastric carcinomas indicates its potential application in the diagnosis and assessment of tumor loads in gastric carcinoma patients.

Adenocarcinoma↗
PubMed1983

The effects of prophylactic expiratory positive airway pressure on the resolution of oleic acid-induced lung injury in dogs.

It is not known whether positive end-expiratory airway pressure (PEEP) merely improves gas exchange in patients with the adult respiratory distress syndrome (ARDS) or if it also affects the resolution of their lung injury. The present investigation was performed to determine whether expiratory positive airway pressure (EPAP), a form of PEEP, is prophylactic in preventing the lung injury induced by oleic acid in dogs or in enhancing its resolution. Arterial and mixed venous blood gases and functional residual capacity (FRC) were measured in 14 pairs of mongrel dogs with indwelling catheters and permanent tracheostomies. One member of each pair was treated with 10 cm H2O EPAP through a valve attached to the tracheostomy tube. Both dogs received 0.06 ml/kg oleic acid intravenously at hour 0. Measurements were made at three, 12, and 24 hours, when EPAP was discontinued, and over the next six days. Five dog pairs were sacrificed at 72 hours; the other surviving animals were sacrificed at 168 hours. FRC was higher at three, 12, and 24 hours in dogs receiving EPAP than in the untreated dogs. The arterial oxygen tension (PaO2) was higher and the venous admixture (Qva/Qt) was lower at three and 12 hours in the dogs receiving EPAP than in the untreated dogs. However, after 24 hours, no differences were noted between the two groups in FRC, PaO2, Qav/Qt, mortality, final lung compliance to initial lung compliance differences, lung water to dry lung weight ratios, or histology. It is concluded that EPAP improves gas exchange during its administration, but has no demonstrable prophylactic effect on the resolution of lung injury in the oleic acid model of human ARDS.

Animals↗
PubMed1981

Indium-111 platelet imaging for detection of platelet deposition in abdominal aneurysms and prosthetic arterial grafts.

Thirty-four platelet imaging studies were performed in 23 patients to determine whether platelet deposition could be detected in patients with vascular aneurysms (18 patients) or in patients in whom Dacron prosthetic grafts had been place (5 patients). In patients in whom abnormal platelet deposition was detected, the effect of administration of platelet-active drugs on platelet deposition was examined. Of the 18 patients with an aneurysm, 12 had positive studies on initial imaging and 2 had equivocally positive images. Of five patients with Dacron arterial grafts in place, four had diffuse platelet deposition in the grafts; the fifth patient had platelet deposition only in a pseudoaneurysm. Eight patients with an abdominal aneurysm and positive or equivocally positive baseline images were restudied during platelet-active drug therapy either with aspirin plus dipyridamole (seven patients) or with sulfinpyrazone (four patients). No patient studied during treatment with aspirin plus dipyridamole had detectably decreased platelet deposition compared with baseline determinations. In contrast, two of four patients studied while receiving sulfinpyrazone showed decreased platelet deposition. Thus, platelet imaging may be of value for studying platelet physiology in vivo and for assessing platelet-active drugs and the thrombogenicity of prosthetic graft materials in human beings.

Abdomen↗
PubMed1981

Dysbaric osteonecrosis: a consequence of intravascular bubble formation, endothelial damage, and platelet thrombosis.

Survival and turnover of platelets, fibrinogen, and plasminogen were measured in association with hyperbaric exposure in man. In addition, kinetic and vascular studies were carried out in a hyperbaric swine model to assess the role of vascular injury and thrombosis in the pathogenesis of dysbaric osteonecrosis. In man, significant increases in platelet and fibrinogen consumption were directly associated with dive depth and with repetitive exposure at lesser depths. The increased destruction of platelets and fibrinogen was not accompanied by reduced blood levels because of compensatory shifts in production rats and distribution between circulating and storage compartments. Platelet consumption was substantially greater than fibrinogen destruction with respect to both severity and duration. Platelet function inhibitors decreased platelet consumption. Increased fibrinogen consumption was sometimes associated with reduced plasminogen survival, but levels of fibrinogen/fibrin degradation products were never measurably altered from normal values. The relationships among platelet and fibrinogen consumption, vascular changes, and dysbaric osteonecrosis were studied in hyperbaric swine. Consumption of hemostatic factors was most severe with rapid, uncontrolled decompression, low oxygen concentrations, and deeper or repetitive dives. Platelet consumption induced by hyperbaric exposure resolved spontaneously with time, suggesting a repair process after the simulated diving conditions were discontinued. Interruption of increased platelet and fibrinogen consumption in the swine model required either moderation of the dive profile or a combination of drugs that inhibit platelet function (dipyridamole or sudoxicam) together with an anticoagulant (warfarin or heparin). Repeated hyperbaric exposure under conditions that uniformly produced femoral osteonecrosis and consumption of platelets and fibrinogen was associated with detectable endothelial injury and arterial intimal lesion formation. Since the diving characteristics of increasing depth and inadequate decompression were associated with both the most severe consumption and the highest frequency of intravascular bubble formation, we postulate that intravascular bubbles, formed during hyperbaria, produce osteonecrosis, perhaps through the following sequence: (1) bubble-related endothelial cell damage; (2) platelet thrombus formation with secondary fibrin deposition; (3) microvascular occlusion; and (4) platelet-dependent arterial narrowing through intimal lesion formation. The role of antithrombotic therapy in the prevention of dysbaric osteonecrosis remains to be determined.

Animals↗
PubMed1980

Human platelets and glomerular basal lamina interaction.

Collagen is one of the major constituents of glomerular basal lamina. Its thrombogenecity has been systematically studied in our laboratory by aggregometry, adenine nucleotide release assay, and electron microscopy. The purified human glomerular basal lamina (HGBL) preparation does not induce platelet degranulation, nucleotide release, or aggregation, although adhesion and spreading of platelets on HGBL are observed. Isolated monomeric HGBL collagen or insoluble HGBL collagen in its native state of organization are similarly inactive. Modification of carbohydrate moieties by sialase, alpha-glucosidase, or sodium periodate oxidation has no effect on HGBL's inability to induce platelet release reaction or aggregation. Therefore, HGBL collagen is not thrombogenic as has been suspected. Adhesion and spreading of platelets on HGBL, which require the noncollagen constituents of HGBL and divalent cations, represent a temporary capillary pavement for endothelial defect distinct from thrombogenic activity of platelets.

Adenine Nucleotides↗
PubMed1980

Structural organization of heterogeneous basal laminas in human glomeruli.

Differential response to 5 M guanidine, pH 7.0, shows at least two classes of glomerular basal laminas: epithelial and endothelial-mesangial. The former is the predominant element, folding into capillary tufts and loops but never completely encircle the entire circumference of glomerular capillaries. It remains as a single, continuous sheet within each glomerulus. The mesangial basal lamina partitions the vascular space into individual capillary lumen. The endothelial basal lamina, which extends from mesangium to encircle capillary lumens, is poorly developed, and undetectable in most capillaries. The organization of these two classes of basal laminas provides a structural framework for understanding glomerular permeability, especially the spatial relationship between capillary lumens and the mesangium. Interruption of the juxtaglomerular epithelial basal lamina, with sprouting of a new endothelial-mesangial bud, and formation of a new glomerular capillary tuft are noted in a group of patients with diabetic glomerulosclerosis and chronic renal failure. Wrinkling and resorption of the juxtamesangial epithelial basal lamina with formation of a new epithelial basal lamina are also observed. These findings indicate that the mesangium and the juxtamesangial epithelial basal lamina may be the active site of glomerular basal lamina resorption, turnover, and neoangiogenesis.

Basement Membrane↗
PubMed1980

The effects of 50% oxygen on the resolution of pulmonary injury.

We studied the effects in dogs of long-term inhalation of 50% oxygen on an 8-day course of pulmonary injury caused by intravenous oleic acid. After lung injury, the experimental animals were placed in an environmental chamber where the inspired oxygen fraction (FIO2) was maintained at 0.5 (N = 12) or 0.21 (N = 12). Oleic acid caused a marked increase in venous admixture and a decreae in PaO2, which persisted at about the same concentration for 3 days after injury. These variables gradually returned toward preinjury values at 8 days. There was no significant difference in the clinical course, gravimetric lung water measurements, or lung histologic findings between oxygen-treated and air-breathing control animals. We concluded that 50% oxygen does not affect either the extent or resolution of lung injury induced by a sublethal dosage of oleic acid.

Animals↗
PubMed1980

The nature of basal lamina alterations in human diabetic glomerulosclerosis.

Studies of human diabetic glomerulosclerosis with a newly devleoped guanidine method have revealed that, like renal tubules, thickening of the glomerular capillary basal lamina is due exclusively to inordinate accumulation of the epithelial basal lamina. There is no excessive deposition of the endothelial basal lamina. Thus, the diabetic nephropathy is characterized by a diffuse thickening of the epithelial basal lamina involving the entire nephron unit, a feature distinct from peripheral diabetic microangiopathy, where the endothelial basal lamina plays a predominant role. The nodular and diffuse mesangial sclerosis is composed of increased mesangial basal lamina, there is no evidence indicating collapsed capillary epithelial basal lamina within Kimmelstiel-Wilson nodules. Hitherto undescribed alterations in the juxtamesangial epithelial basal lamina suggesting new glomerular capillary tuft formation are also presented.

Capillaries↗
PubMed1979

Basal lamina heterogeneity in the glomerular capillary tufts of human kidneys.

Two classes of glomerular basal laminas are identified with a newly developed guanidine technique. The electron-opaque epithelial basal lamina is the most prominent element of the glomerular basal lamina scaffold. It is a continuous layer within each glomerulus, folding into capillary tufts and loops, but never completely encircling the entire circumference of each capillary, similar to the serosa covering the intestinal loop and mesentery. The vascular space so defined is further partitioned into individual capillary lumen by an electron-lucent mesangial basal lamina, that forms a meshwork continuous with the vascular pole of the glomerulus and extends peripherally to surround capillary lumens. The latter, designated endothelial basal lamina, is extremely attenuated and appears as a vestigial structure in glomerular capillary loops. Changes in juxtamesangial epithelial basal lamina indicate that it may be the site of the bulk removal and renewal of the epithelial basal lamina. The unique epithelial origin of glomerular capillary basal lamina and its organization provide a structural basis for understanding the glomerular physiology gained by various tracer studies. The results also suggest that the guanidine technique may be a useful new approach to the analysis of basal lamina alterations in various glomerular diseases.

Aged↗
PubMed1979

Angioimmunoblastic lymphadenopathy with retinitis and drug related exacerbations: a clinicopathological case study.

A patient with angioimmunoblastic lymphadenopathy with dysproteinemia was followed over a three year period from diagnosis to death. He presented with arthralgias, uveitis and respiratory insufficiency and developed hyperuricemic renal failure upon institution of treatment. Aggressive combination chemotherapy was required to reverse progressive thrombocytopenia and pulmonary involvement. A complete remission was achieved twice. There was a striking temporal relationship between the administration of antibiotics or allopurinol and exacerbations of the disease. Hypocomplementemia and transient evidence of vasculitis suggested the presence of immunecomplexes. Serial lymph node biopsies showed the progression of this disorder from a pleomorphic immunoblastic proliferation to a lymphocyte-depleted, fibrotic process, in parallel with a decline from hyper- to hypogammaglobulinemia. This case illustrates the broad clinical spectrum of angioimmunoblastic lymphadenopathy with dysproteinemia and suggests that aggressive treatment is necessary in selected patients.

Agammaglobulinemia↗
PubMed1979

Basal lamina of alveolar epithelium and capillaries: quantitative changes with aging and in diabetes mellitus.

Epithelial and capillary basal laminae (BL) of alveoli are significantly thicker in diabetics than they are in age-matched control subjects. The degree of thickening does not correlate significantly with patient age or with known duration of diabetes. The thickness of both types of BL in the lungs correlates significantly with thickness of BL in renal tubules and muscle capillaries. However, in muscle capillaries and in renal tubules, the BL deposits are 5 to 10 times greater than they are in the lungs. The effects of BL changes on pulmonary function remain to be explored.

Adolescent↗
PubMed1978

Fluid leaks from extra-alveolar vessels in living dog lungs.

Edema transudation from extra-alveolar vessels was investigated in anesthetized, open-chested dogs. Fluid accumulation at different alveolar and extra-alveolar vascular pressures was assessed by continuous lung weighing and microscopy. The left (experimental) lung was distended with 6% CO2 and air while normal arterial blood gases were maintained by separately ventilating the right lung. Extra-alveolar vessels were isolated by compressing alveolar vessels with alveolar pressures high enough to stop blood flow. Weight increased steadily (edemogenesis) when pulmonary arterial and/or pulmonary venous pressure was 1 cmH2O below this pressure. Because some alveolar vessels at the lung base could have remained open and leaked, extra-alveolar vessels were also separated from alveolar vessels by glass bead embolization sufficient to stop perfusion. Lung weight gains followed selective pulmonary arterial or venous pressure elevations. Electron microscopy demonstrated edema in experimental lobes which was not present in control lobes with undistended extra-alveolar vessels at the same alveolar pressure. Thus pulmonary edema can be caused by fluid leaking from extra-alveolar vessels.

Animals↗
PubMed1978

Mechanisms of platelet adhesion to the basal lamina.

The human glomerular basal lamina (HGBL) is composed of collagenous and noncollagenous glycoproteins. We assessed the role played by each costituent in platelet-basal-lamina interaction by selective cleavage and removal of each component by clostridial collagenase or by pepsin. When noncollagenous proteins are removed from HGBL, human platelets exhibit littel reactivity toward the residual collagen framework of the isolated basal lamina. With the noncollagen matrix of basal lamina, after removal of the bulk of the collagen, platelet adhesion and spreading proceed normally in the presence of divalent cations, similar to what occurs on intact basal lamina. No platelet degranulation or aggregation is observed. The results indicate that the basal lamina collagen, even in its native packing arrangement, lacks affinity for platelet adhesion and is incapable of triggering platelet release reactions. Platelet adhesion and spreading on the basal lamina appears to depend primarily on the presence of the noncollagen components and to require divalent cations. The data suggest the presence on platelets of receptors for basal lamina distinct from those for interstitial collagens. These receptors activate a unique modulation of platelet behavior, ie, adhesion and spreading without degranulation. A difference in biologic function of the basal lamina and interstitial collagens is apparent in these experiments.

Collagen↗