Seminal vesicle cystic dilatation masquerading as proctalgia fugax.
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Adult↗
Biomedical subjects
A Khan
Publications and source records attributed to A Khan.
Cloning of bacterial genes specifying degradation of 4-chlorobiphenyl from Pseudomonas putida OU83.
Genes capable of 4-chlorobiphenyl (4-CBP) degradation were cloned from 4-CBP-degrading Pseudomonas putida OU83 by using a genomic library which was constructed in the broad-host-range cosmid vector pCP13. P. putida AC812 containing chimeric cosmid-expressing enzymes involved in the 4-CBP degradation pathway were identified by detecting 3-phenylcatechol dioxygenase activity (3-PDA). Chimeric cosmid clones pOH83, pOH84, pOH85, pOH87, and pOH88 positive for 3-PDA grew in synthetic basal medium containing 4-CBP (5 mM) as a carbon source. Restriction digestion analysis of recombinant cosmids showed DNA inserts ranging from 6 to 30 kilobase pairs. Southern hybridization data revealed that the cloned DNA inserts originated from strain OU83. Gas chromatography-mass spectrometry analysis of the metabolites of P. putida AC812(pOH88) incubated with 4-CBP and 4'-chloro-3-phenylcatechol showed the formation of 4-chlorobenzoic acid and benzoic acid. These results demonstrate that the cloned DNA fragments contain genes encoding for chlorobiphenyl dioxygenase (cbpA), dihydrodiol dehydrogenase (cbpB), 4'-chloro-3-phenylcatechol dioxygenase (cbpC), a meta-cleavage compound (a chloro derivative of 2-hydroxy-6-oxo-6-phenylhexa-2,4-dienoate) hydrolase (cbpD), and a new dechlorinating activity (dcpE). The location of the cbpC gene specifying 3-PDA was determined by subcloning an EcoRI DNA fragment (9.8 kilobase pairs) of pOH88 in plasmid vector pUC19. The cloned gene encoding 3-PDA was expressed in Escherichia coli HB101 and had substrate specificity only for 3-phenylcatechol and 4'-chloro-3-phenylcatechol.
Biodegradation, Environmental↗
Pulmonary parenchymal disease: evaluation with high-resolution CT.
Usefulness of high-resolution computed tomography (HRCT) in locating pulmonary parenchymal disease in relation to the pulmonary lobule was evaluated in 71 patients, including 30 with normal pulmonary parenchyma and 41 with various pulmonary diseases. Both 10-mm-thick sections and 1.5- or 3.0-mm-thick HRCT scans were obtained. Distribution of pulmonary parenchymal disease was classified as centrilobular, panlobular, perilobular, bronchovascular, or nonlobular. Intralobular classification of disease distribution was more feasible in less severely diseased regions. HRCT revealed thickened intralobular bronchovascular bundles in patients with bronchiolitis obliterans, mycoplasma pneumonia, and pulmonary tuberculosis and thickening of both bronchovascular bundles and perilobular structures in patients with sarcoidosis, lymphangitis carcinomatosa, and malignant lymphoma. Centrilobular areas of increased attenuation were seen in patients with bronchopneumonia and pulmonary cryptococcosis. Centrilobular emphysema and bronchiolectasis were recognized only on HRCT images. The improved clarity and sharpness of parenchymal abnormalities on HRCT images, even in severely involved areas, provide additional information about disease distribution.
Female↗
Glucose turnover in hyperthyroid patients with normal glucose tolerance.
To determine the diabetogenic effect(s) of thyroid hormones, we simultaneously measured glucose turnover in six hyperthyroid patients and six normal subjects. All had normal fasting blood glucose concentration and oral glucose tolerance test values. We determined hepatic total glucose output (HTGO) and total glucose phosphorylation with [2-3H]glucose and hepatic glucose production (HGP) and irreversible glucose uptake using [6-3H]glucose. The difference between the two turnover rates indicates the extent of hepatic glucose cycling (glucose in equilibrium glucose-6-phosphate). Measurements were made both in the postabsorptive steady state and during a 2-h glucose infusion (11.1 mumol/kg.min). The postabsorptive HTGO and total glucose phosphorylation were increased in the hyperthyroid patients [13.5 +/- 0.8 (+/- SE) vs. 11.3 +/- 0.4 mumol/kg.min; P less than 0.05]. HGP and irreversible glucose uptake also were slightly but not significantly higher. During the glucose infusion, HTGO and HGP were less suppressed in the hyperthyroid patients than in the normal subjects, while the increments in peripheral glucose uptake were normal. In hyperthyroidism, glucose cycling was increased both postabsorptively (2.35 +/- 0.27 vs. 1.17 +/- 0.25 mumol/kg.min; P less than 0.025) and during glucose infusion (2.57 +/- 0.34 vs. 1.31 +/- 0.35 mumol/kg.min; P less than 0.05). We conclude that increases in HTGO and HGP are important features of hyperthyroidism, especially during glucose infusion. The increase in GC indicates increased activities of both glucokinase and glucose-6-phosphatase. The diabetogenic effect of hyperthyroidism, as revealed most markedly by [2-3H]glucose, could be accounted for by augmented glucose production, possibly due to increased glucose-6-phosphatase activity.
Adult↗
Cerebrospinal fluid beta 2 microglobulin in patients infected with human immunodeficiency virus.
We prospectively evaluated CSF concentrations of beta 2 microglobulin (beta 2M) in 65 human immunodeficiency virus type 1 seropositive patients. The highest concentrations occurred in those with lymphoma, neurologic opportunistic infections, and acquired immune deficiency syndrome dementia complex (ADC). There was a high correlation between the CSF beta 2M concentration and ADC severity, suggesting that CSF beta 2M may be useful as a marker for the development, progression, and perhaps response to treatment of ADC. Elevated CSF beta 2M was not due to CSF pleocytosis and was usually independent of blood-brain barrier dysfunction.
Acquired Immunodeficiency Syndrome↗
Dissociation of AIDS-related vacuolar myelopathy and productive HIV-1 infection of the spinal cord.
Although merging clinically within the spectrum of the AIDS dementia complex, vacuolar myelopathy is a pathologically distinct entity detected in up to 30% of autopsied patients succumbing to the late complications of human immunodeficiency virus type 1 (HIV-1) infection. Using immunohistochemistry and in situ hybridization to detect an HIV-1 core protein and viral mRNA, respectively, in tissue sections, and culture isolation to assess infectious virus in tissue homogenates, we found that vacuolar myelopathy was independent of productive HIV-1 infection of the spinal cord and brain. These results indicate that AIDS-associated vacuolar myelopathy is either not related directly to spinal cord HIV-1 infection or involves nonproductive infection and pathobiological processes distinct from those responsible for the multinucleated-cell inflammatory infiltrates that serve as histopathologic markers of productive CNS HIV-1 infection.
Acquired Immunodeficiency Syndrome↗
Cutaneous nerves of the embryonic chick wing do not develop in regions denuded of ectoderm.
Peripheral nerves travel to their targets along precise routes, and it is likely that different cues provide guidance at different stages of the journey. In a developing chick limb, the cutaneous nerve fibres follow at first deep mixed nerve trunks, in company with motor axons; they branch from these trunks at predictable points and approach the skin; they then ramify profusely to form a plexus at a precisely defined depth beneath the ectoderm, at exactly the same level as the blood vascular plexus. To analyse the role of signals from the target patch of skin in regulating cutaneous nerve development, we have ablated patches of dorsal wing ectoderm using short-wave ultraviolet irradiation at E4 (embryonic day 4), approximately one day before nerves grow into the limb bud. The irradiated patches remain denuded of ectoderm for more than a week, by which time the cutaneous nerve plexus on the contralateral control side is well developed and can be revealed by whole-mount silver staining. Where the ectoderm has been ablated, no cutaneous nerve plexus forms, and the nerve branches that normally would have diverged from the neighbouring mixed nerve trunk to innervate the missing patch of skin are absent - ab initio, apparently. The routes of the mixed nerve trunks are not affected. Partial ablation of the territory of a cutaneous nerve branch often leads to loss of the whole nerve branch; the intact skin territory thus left vacant is invaded by ramifications from the remaining cutaneous branches, as expected if the normal extent of a cutaneous nerve's territory is regulated by competition. Where there is an ectodermal lesion, cutaneous innervation stops precisely at its boundary, even though the vascular plexus extends for some distance beyond this margin, beneath the denuded surface. The data suggest that the embryonic skin is required firstly to trigger divergence of cutaneous nerve branches from the mixed nerve trunks, and secondly, once the nerve fibres have reached the skin, to supply a trophic cue (probably NGF) encouraging growth of a plexus; at the same time, the embryonic skin generates a signal inhibiting nerves from approaching closer than about 70 microns to the surface.
Animals↗
[Studies on acute toxicity and serum level changes of tumor necrosis factor].
BALB/C female mice were given different dosages of TNF in 0.1 ml sterile PBS containing 1% human serum albumin. Control mice were injected with PBS and human albumin alone. Autopsy examination was carried out and blood biochemistry studied. The results showed that the LD50 was 6 X 10(7) mu/kg. There were serious hyperemia and inflammation of the organs of dead mice, while other smaller dosages of TNF caused acute toxicity of different degrees, except for the 3 X 10(6) mu/kg dosage. Changes of alkaline phosphatase were significant compared with control. Blood sugar increases correlated with the TNF dosage. Changes of GPT and BUN were insignificant. TNF levels in the sera of humans and rabbits were also studied following TNF injection. The serum level of TNF decreased rather quickly in both animals and patients: about 85% of TNF was lost within 5 min after TNF injection, and no TNF could be detected 6 hrs after injection.
Alkaline Phosphatase↗
Variable presentations of medullary carcinoma of the thyroid gland.
Although medullary carcinoma of the thyroid is rare, this disease generates considerable interest due to its unusual cellular origin from parafollicular C cells, ability to secrete calcitonin, and association with other endocrine adenomatosis. Pentagastrin-calcium stimulation continues to be the most valuable test for early diagnosis, in detecting recurrence of tumor, and for screening of family members. Total thyroidectomy along with central neck dissection is the treatment of choice. However, management of metastatic disease in the lateral neck remains controversial. We report three cases of medullary carcinoma of the thyroid to illustrate its various forms and the use of diagnostic tests.
Adult↗
Chronic intussusception in a young adult with cystic fibrosis.
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Adolescent↗
Comparison of CT and chest radiographs in the evaluation of post-therapy lymphoma patients.
A comparative study of the efficacy of thoracic CT (TCT) and chest radiograph for the assessment of complete remission, residual or recurrent disease, was undertaken on 31 post-therapy lymphoma patients (23 Hodgkin's, 8 non-Hodgkin's). The TCT and chest radiograph were evaluated independently. Compared with the chest CT, the sensitivity of the chest radiograph was low (56%). The confidence level of abnormal findings on the chest radiograph was lower, Additional diagnostic information provided by TCT influenced the clinical management in 33% of the cases. Compared with the chest radiograph, TCT had a higher diagnostic and management efficacy at the follow-up evaluation of post-therapy lymphoma patients.
Combined Modality Therapy↗
Pneumobelt for sleep in the ventilator user: clinical experience.
A pneumobelt with a positive pressure respirator was used for sleep for three patients with chronic respiratory insufficiency secondary to syringomyelia, poliomyelitis, and Friedreich's ataxia respectively. This device was found to be effective in improving and maintaining their daily functioning in the community or institute.
Chronic Disease↗
Pulmonary disease in progressive systemic sclerosis. A complication of gastroesophageal reflux and occult aspiration?
Thirteen patients with progressive systemic sclerosis were studied to evaluate the possible role of gastroesophageal reflux as a contributing pathogenic factor in the pulmonary disease of the patients. The evaluation of all patients included fiberoptic esophagogastroduodenoscopy with biopsies of the esophagus, otolaryngologic evaluation, technetium Tc 99m sulfur colloid aspiration scan, pulmonary function testing, including the diffusing capacity for carbon monoxide (DLCO) test, and 24-hour intraesophageal pH monitoring with probes placed 5 and 15 cm above the lower esophageal sphincter. Eleven patients had microscopic and macroscopic evidence of proximal esophagitis, 12 patients had laryngeal changes suggestive of aspiration, and 12 patients had abnormal DLCO values. Using multiple regression analysis, the degree of DLCO impairment correlated with the proximal and distal reflux episodes and scores recorded by pH monitoring. There was direct and indirect evidence for proximal gastroesophageal reflux and aspiration in the majority of patients, and a distinct correlation between the severity of reflux and the severity of pulmonary disease. Aggressive antireflux therapy may be helpful in reducing the pulmonary damage due to aspiration in these patients.
Adult↗
Human natural cytotoxic activity mediated by tumor necrosis factor: regulation by interleukin-2.
Freshly obtained normal lymphoid cells kill certain tumor target cells in vitro. Using peripheral blood lymphocytes (PBLs) and the human tumor target cell line BT-20, we have defined a tumor necrosis factor (TNF)-dependent, cell-mediated cytotoxic mechanism that is homologous to the murine natural cytotoxic (NC) cell activity. Human NC cell activity was detected in freshly isolated PBLs and was augmented by short in vitro pulses with recombinant human interleukin-2 but not with recombinant human alfa interferon. Monoclonal anti-TNF antibodies inhibited the killing of the target cells. The independence of interferon and the mediation of killing by TNF distinguish human NC cell activity from natural killer and lymphokine-activated killer cell activities.
Cells, Cultured↗
Human cytokines, tumor necrosis factor, and interferons: gene cloning, animal studies, and clinical trials.
Presented is a comprehensive program designed to isolate human cytokine genes and investigate their relative induction, and to analyze cytokine activities in cell culture, animal tumor models, and human clinical trials. Human cytokine cDNAs have been isolated from a cDNA library made from normal human peripheral blood leukocytes (PBLs) treated with Sendai virus and the relative induction of tumor necrosis factor (TNF), alpha and gamma interferons (IFN-alpha, IFN-gamma), and interleukin-1 beta IL-1 beta) genes has been analyzed. In the Sendai virus-induced PBL system, IL-1 beta mRNA was shown to be approximately twofold higher than TNF or IFN-alpha mRNA whereas IFN-gamma mRNA was 50-100-fold lower than TNF or IFN-alpha mRNA. The cytotoxic activity of TNF was analyzed on several cell lines and IFN-alpha and IFN-gamma were shown to potentiate TNF cytotoxicity about 2-200-fold depending on cell lines. The LD50 for recombinant TNF in BALB/c mice was determined to be 6 X 10(7) U/kg and the therapeutic dose of recombinant TNF in sarcoma 180 bearing BALB/c mice was 3 X 10(5) U/kg, indicating a wide therapetic index. Phase I clinical trials of recombinant TNF given I.V. indicated a tolerated dose of 150,000 U/kg with biphasic half-life (T-1/2) of 2 and 31 min following TNF injection. Phase II trials of TNF and trials of TNF combined with IFN-alpha are in progress. These studies indicate that cytokines such as TNF and IFN-alpha are subject to similar induction systems, potentiate each other's activities, and can be tolerated at specific doses for potential therapeutic use.
Animals↗
Hospitalization effect in acute mania.
We studied 31 patients meeting DSM-III criteria for bipolar affective disorder, manic type. All were treated in hospital, 18 on an open ward and 13 on a psychiatric intensive-care unit. Despite the use of only moderate doses of medication, dramatic clinical improvement was observed over the first 48 hours of treatment using the Brief Psychiatric Rating Scale and Beigel Mania Rating Scale as objective rating measures. Significantly greater improvement occurred in the psychiatric intensive-care unit in comparison to the open ward. We suggest that hospitalization effect is of prime importance in the early management of the acutely manic patient.
Adult↗
Monoclonal antibodies against human recombinant tumor necrosis factor: prevention of endotoxic shock.
Six murine monoclonal antibodies, AT-1, 2, 3, 4, 5, and 6 were produced against human recombinant tumor necrosis factor (gamma TNF). AT-1, -2, -3, -4, and -6 were IgG1, and AT-5 was IgG2a. AT-1, -2, and -3 neutralized the activity of gamma TNF (2 X 10(3) U/ml) over a range of dilutions between 5 and 500 micrograms/ml of IgG, while AT-4, -5 and -6 failed to neutralize the activity in these concentrations. All the antibodies showed immunoprecipitating activity for gamma TNF (2 X 10(3) U/ml) over a range of dilutions between 0.5 and 500 micrograms/ml. The AT-6 was weaker than the rest. AT-1, which neutralized gamma TNF activity efficiently, and AT-4, which did not neutralize the activity, were used to protect mice against endotoxic shock. AT-1 protected mice from the lethal effects of endotoxin, while AT-4 failed to do so. AT-1, -2, and -3 also neutralized the activity of human and mouse natural TNF. AT-1, -2, and -3 neutralized the activity of gamma TNF, but not that of lymphotoxin (LT) and interferon (IFN).
Animals↗