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Biomedical subjects

Q Yang

Publications and source records attributed to Q Yang.

At least 109 records · Page 6Linked to original sources
PubMed2001

Prostaglandin E(2) increases cyclic AMP and inhibits endothelin-1 production/secretion by guinea-pig tracheal epithelial cells through EP(4) receptors.

Prostaglandin E(2) (PGE(2)) increased adenosine 3' : 5'-cyclic monophosphate (cyclic AMP) formation in tracheal epithelial cells and concomitantly decreased the production/secretion of immunoreactive endothelin (irET). Naturally occurring prostanoids and selective and non-selective EP receptor agonists showed the following rank order of potency in stimulating cyclic AMP generation by epithelial cells: PGE(2) (EP-selective)>16,16-dimethyl PGE(2) (EP-selective)>11-deoxy PGE(2) (EP-selective)>>>iloprost (IP/EP(1)/EP(3)-selective), butaprost (EP(2)-selective), PGD(2) (DP-selective), PGF(2alpha) (FP-selective). The lack of responsiveness of the latter prostanoids indicated that the prostanoid receptor present in these cells is not of the DP, FP, IP, EP(1), EP(2) or EP(3) subtype. Pre-incubating the cells with the selective TP/EP(4)-receptor antagonists AH23848B and AH22921X antagonized the PGE(2)-evoked cyclic AMP generation. This suggested that EP(4) receptors mediate PGE(2) effects. However, in addition to any antagonistic effects at EP(4)-receptors, both compounds, to a different extent, modified cyclic AMP metabolism. The selective EP(1), DP and EP(2) receptor antagonist (AH6809) failed to inhibit PGE(2)-evoked cyclic AMP generation which confirmed that the EP(2) receptor subtype did not contribute to the change in cyclic AMP formation in these cells. The PGE(2)-induced inhibition of irET production by guinea-pig tracheal epithelial cells was due to cyclic AMP generation and activation of the cyclic AMP-dependent protein kinase since this effect was reverted by the cyclic AMP antagonist Rp-cAMPS. These results provide the first evidence supporting the existence of a functional prostaglandin E(2) receptor that shares the pharmacological features of the EP(4)-receptor subtype in guinea-pig tracheal epithelial cells. These receptors modulate cyclic AMP formation as well as ET-1 production/secretion in these cells.

Adenosine↗
PubMed2001

Inhibition of vasoconstriction by AJ-2615, a novel calcium antagonist with alpha(1)-adrenergic receptor blocking activity in human conduit arteries used as bypass grafts.

AIMS: Graft spasm may develop during coronary artery bypass grafting and reversal of spasm is still challenging. The purpose of this study was to investigate the in vitro vascular relaxant properties of AJ-2615 in human internal mammary artery (IMA). METHODS: We studied 264 IMA rings taken from 65 patients undergoing coronary artery bypass grafting surgery with organ bath technique. The interaction between AJ-2615 and various vasoconstrictors was investigated in two ways. RESULTS: AJ-2615 caused complete relaxation in methoxamine-contracted IMA rings (100.0+/-0.0%; n = 8) and nearly full relaxation in potassium chloride-contracted IMA rings (91.4+/-5.7%; n = 8) or noradrenaline-contracted IMA rings (89.3+/-2.8%; n = 8). AJ-2615 also induced remarkable relaxation in IMA rings contracted by other vasoconstrictors. In comparison with the alpha1-adrenoceptor antagonist prazosin, AJ 2615 showed similar maximal relaxation in IMA rings contracted by methoxamine or norepinephrine. On the other hand, incubation with AJ-2615 (0.1-1 microM) significantly inhibited all the vasoconstrictor-mediated vasoconstriction except endothelin-1 in a concentration-dependent manner. CONCLUSIONS: The results suggested that in human IMA, AJ-2615 has an inhibitory effect on vasoconstriction mediated by a variety of vasoconstrictors and the mechanism of relaxation may be related to its calcium antagonism and alpha1-adrenergic receptor blocking activity. AJ-2615 may have important clinical implications for patients undergoing coronary artery bypass surgery for reversing and preventing graft spasm.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2001

Malignant endocrine tumors in patients with MEN 1 disease.

BACKGROUND: In contrast with multiple endocrine neoplasia type 2, malignancies are of minor importance in multiple endocrine neoplasia type 1 (MEN 1) syndrome. METHODS: The data for 42 patients with MEN 1 syndrome were evaluated. Twelve patients (29%) had 1 or more associated malignancies: malignant gastrinoma (1 patient), neuroendocrine tumors of the thymus (2 patients), neuroendocrine tumors of the lung (3 patients), neuroendocrine tumor of the ileum (1 patient), adrenocortical carcinomas (2 patients), and a combination of neuroendocrine tumors of thymus, lung or pancreas (3 patients). RESULTS: Despite suspected MEN 1 syndrome in 7 patients, malignancies were detected late in 4 patients and could not be resected curatively. The survival rates for 5 years and 10 years after operation of the malignant tumor were 66% +/- 14% (SE) and 33% +/- 15% (SE), respectively. CONCLUSIONS: In patients at risk for the MEN 1 syndrome, genetic screening is indispensable. Gene carriers have to be followed up closely with hormone analysis and routine examination of the thorax, pancreas, and adrenal glands to detect malignancies as early as possible.

Adolescent↗
PubMed2001

Long-term biochemical results after operative treatment of primary hyperparathyroidism associated with multiple endocrine neoplasia types I and IIa: is a more or less extended operation essential?

OBJECTIVE: To analyse our long term results in patients operated on for primary hyperparathyroidism associated with multiple endocrine neoplasia types I and IIa. DESIGN: Retrospective (data collection) and prospective (follow-up) analysis. SETTING: University hospital, Germany. SUBJECTS: 39 patients with MEN type I-associated and 7 patients with MEN-type-IIa-associated primary hyperparathyroidism. INTERVENTIONS: Subtotal parathyroidectomy (n = 25 with MEN I and 1 with MEN IIa), total parathyroidectomy and autotransplantation (one in each group) and removal of only enlarged glands (13 with MEN type I and 5 with MEN type IIa). MAIN OUTCOME MEASUREMENTS: Recurrence rate of hyperparathyroidism and permanent hypocalcaemia postoperatively. RESULTS: Subtotal parathyroidectomy in patients with MEN type I gave a significantly lower recurrence rate than removal of only enlarged glands (3/25 compared with 3/13, log rank, p = 0.04). Permanent hypocalcaemia developed in 3/25 compared with 3/13, respectively. 2/5 patients with MEN type IIa developed recurrences after removal of only enlarged glands and the rate was higher than expected. CONCLUSIONS: A more extensive operation is essential for patients with MEN type I; the rate of permanent hypocalcaemia is not increased, but the recurrence rate is reduced. Patients with MEN type IIa should be treated by excision of enlarged glands alone, but this may be extended to subtotal parathyroidectomy in patients with severe symptoms.

Adenoma↗
PubMed2001

Pneumatic lithotripsy versus laser lithotripsy in the endoscopic treatment of ureteral calculi.

PURPOSE: To compare the efficacy, safety, and features of pneumatic lithotripsy (PL) with those of laser lithotripsy (LL) and present our clinical experience in the endoscopic management of ureteral calculi. PATIENTS AND METHODS: From August 1994 to February 2000, 285 consecutive patients underwent endoscopic lithotripsy with either the Swiss Lithoclast pneumatic lithotripter (145 patients) or the Ho:YAG laser lithotripter (140 patients) for the treatment of ureteral calculi. RESULTS: In one single session, the overall successful stone fragmentation rate of LL was higher than that of PL (95.7% v 69.7%; P < 0.01). The average time to stone-free status was shorter for LL than for PL (18 days v 31 days; P < 0.01). No major complications were observed in LL, while five ureteral perforations were encountered in PL. CONCLUSIONS: Laser lithotripsy has advantages over PL in high efficiency of stone fragmentation and a low complication rate. Laser lithotripsy is a powerful, effective, and safe treatment modality for ureteral calculi.

Adolescent↗
PubMed2001

Abnormal axonal inward rectifier in streptozocin-induced experimental diabetic neuropathy.

In order to explore the pathophysiology of diabetic neuropathy, we studied serial changes of axonal excitability in 20 adult Wistar rats with streptozocin-induced diabetes using the technique of threshold electrotonus (TE). After persistent hyperglycaemia had developed, rats were divided into two groups: nine were fed a diet containing aldose reductase inhibitor (Epalrestat 30 mg/kg/day) (ARI(+) group) and 11 were fed a diet without the inhibitor (ARI(-) group). Eight normal control rats of similar age (NC group) were also studied. We monitored membrane properties of motor axons in the tail for 3 months using TE to measure the changes in excitability induced by subthreshold polarizing currents while recording compound muscle action potentials (CMAPs) in the tail muscle. The ARI(-) group showed a significant increase in CMAP latency 1 month after streptozocin injection, and by 3 months there was significantly lower excitability after hyperpolarization for 100 ms compared with the NC group. A similar change in TE was reproduced by injection of caesium chloride, an inhibitor of inward rectification. By contrast, the ARI(+) group exhibited no significant change in TE or latency at 3 months, although they showed significant body weight loss and hyperglycaemia. These findings indicate that inward rectification is reduced in an experimental model, as in human diabetes, and that blocking the polyol pathway with an ARI prevents this reduction. Reduced inward rectification potentiates conduction block caused by activity-dependent hyperpolarization and may underlie the decreased vibratory sensation seen in the early stage of diabetic neuropathy.

Action Potentials↗
PubMed2001

Rejection of S-heteroallelic pollen by a dual-specific s-RNase in Solanum chacoense predicts a multimeric SI pollen component.

S-heteroallelic pollen (HAP) grains are usually diploid and contain two different S-alleles. Curiously, HAP produced by tetraploids derived from self-incompatible diploids are typically self-compatible. The two different hypotheses previously advanced to explain the compatibility of HAP are the lack of pollen-S expression and the "competition effect" between two pollen-S gene products expressed in a single pollen grain. To distinguish between these two possibilities, we used a previously described dual-specific S(11/13)-RNase, termed HVapb-RNase, which can reject two phenotypically distinct pollen (P(11) and P(13)). Since the HVapb-RNase does not distinguish between the two pollen types (it recognizes both), P(11)P(13) HAP should be incompatible with the HVapb-RNase in spite of the competition effect. We show here that P(11)P(13) HAP is accepted by S(11)S(13) styles, but is rejected by the S(11/13)-RNase, which demonstrates that the pollen-S genes must be expressed in HAP. A model involving tetrameric pollen-S is proposed to explain both the compatibility of P(11)P(13) HAP on S(11)S(13)-containing styles and the incompatibility of P(11)P(13) HAP on styles containing the HVapb-RNase.

Alleles↗
PubMed2001

Assembly, annotation, and integration of UNIGENE clusters into the human genome draft.

The recent release of the first draft of the human genome provides an unprecedented opportunity to integrate human genes and their functions in a complete positional context. However, at least three significant technical hurdles remain: first, to assemble a complete and nonredundant human transcript index; second, to accurately place the individual transcript indices on the human genome; and third, to functionally annotate all human genes. Here, we report the extension of the UNIGENE database through the assembly of its sequence clusters into nonredundant sequence contigs. Each resulting consensus was aligned to the human genome draft. A unique location for each transcript within the human genome was determined by the integration of the restriction fingerprint, assembled genomic contig, and radiation hybrid (RH) maps. A total of 59,500 UNIGENE clusters were mapped on the basis of at least three independent criteria as compared with the 30,000 human genes/ESTs currently mapped in Genemap'99. Finally, the extension of the human transcript consensus in this study enabled a greater number of putative functional assignments than the 11,000 annotated entries in UNIGENE. This study reports a draft physical map with annotations for a majority of the human transcripts, called the Human Index of Nonredundant Transcripts (HINT). Such information can be immediately applied to the discovery of new genes and the identification of candidate genes for positional cloning.

Alleles↗
PubMed2001

Effects of Choto-san on microcirculation, serum nitric oxide and lipid peroxides in patients with asymptomatic cerebral infarction.

The effects of Choto-san on microcirculation, serum nitric oxide and lipid peroxides were investigated. Fifteen patients with asymptomatic cerebral infarction were investigated before and after a four-week administration of Choto-san. The variables of microcirculation of the bulbar conjunctiva, which were the internal diameter of vessels, flow velocity and flow volume rate, were increased. Serum NO2(-)/NO3(-) tended to increase and lipid peroxides were decreased. Total serum cholesterol was also decreased. These results suggest that Choto-san may improve microcirculation affected by endothelial function and fat metabolism.

Blood Flow Velocity↗
PubMed2001

Melatonin potentiates contractile responses to serotonin in isolated porcine coronary arteries.

The present study was designed to determine the effects of melatonin on coronary vasomotor tone. Porcine coronary arteries were suspended in organ chambers for isometric tension recording. Melatonin (10(-10)-10(-5) M) itself caused neither contraction nor relaxation of the tissues. Serotonin (10(-9)-10(-5) M) caused concentration-dependent contractions of coronary arteries, and in the presence of melatonin (10(-7) M) the maximal response to serotonin was increased in rings with but not without endothelium. In contrast, melatonin had no effect on contractions produced by the thromboxane A(2) analog U-46619 (10(-10)-10(-7) M). The melatonin-receptor antagonist S-20928 (10(-6) M) abolished the potentiating effect of melatonin on serotonin-induced contractions in endothelium-intact coronary arteries, as did treatment with 1H-[1, 2,4]oxadiazolo[4,3-a]quinoxalin-1-one (10(-5) M), methylene blue (10(-5) M), or N(G)-nitro-L-arginine (3 x 10(-5) M). In tissues contracted with U-46619, serotonin caused endothelium-dependent relaxations that were inhibited by melatonin (10(-7) M). Melatonin also inhibited coronary artery relaxation induced by sodium nitroprusside (10(-9)-10(-5) M) but not by isoproterenol (10(-9)-10(-5) M). These results support the hypothesis that melatonin, by inhibiting the action of nitric oxide on coronary vascular smooth muscle, selectively potentiates the vasoconstrictor response to serotonin in coronary arteries with endothelium.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2001

Adenylyl cyclase isoforms and signal integration in models of vascular smooth muscle cells.

Adenylyl cyclases present a potential focal point for signal integration in vascular smooth muscle cells (VSMC) influencing contractile state and cellular responses to vessel wall injury. In the present study, we examined the influence of the vasoactive peptide arginine vasopressin (AVP) on cAMP regulation in primary cultures of rat aortic VSMC and in the A7r5 arterial smooth muscle cell line. In cultured VSMC and A7r5 cells, AVP had no effect on basal cAMP but differentially affected beta-adrenergic receptor-induced activation of adenylyl cyclase. AVP synergistically increased (twofold) isoproterenol-stimulated cAMP production in VSMC but inhibited the effect of isoproterenol (50%) in the A7r5 cell line. The effects of AVP in both preparations were blocked when cells were pretreated with a selective V(1) vasopressin receptor antagonist. Moreover, the actions of AVP in both models were dependent on release of intracellular Ca(2+) and were mimicked by elevation of Ca(2+) with the ionophore A23187, suggesting that the responses to AVP involve Ca(2+)-mediated regulation of adenylyl cyclase stimulation. Adenylyl cyclase types I, III, and VIII are stimulated by Ca(2+)/calmodulin, whereas types V and VI are directly inhibited by Ca(2+). RNA blot analysis for effector isotypes indicated that both VSMC and A7r5 cells expressed types III, V, and VI. VSMC also expressed mRNA for type IV and VIII effectors, which could account for the cell-specific responses to peptide hormone and Ca(2+).

Adenylyl Cyclases↗
PubMed2001

Spatiotemporal properties of an evoked population activity in rat sensory cortical slices.

We have examined the spatiotemporal properties of ensemble activity, an evoked all-or-none polysynaptic activity in rat neocortical slices. Ensemble activity occurred in cortical slices bathed in normal artificial cerebrospinal fluid (ACSF) and was evoked by a single electrical shock either to the white matter or directly to the cortical tissue. This activity was seen in slices of somatosensory and auditory cortices; in other cortical areas we have not been able to evoke it. The activity developed 10 to 250 ms poststimulus and lasted 280 +/- 120 ms in local field potential (LFP) recordings. Voltage-sensitive dye imaging showed that this activity was an area of activation 0.8 +/- 0.4 mm wide that propagated slowly (11.4 +/- 6.2 mm/s, n = 60, 6 animals) in the horizontal direction. Due to this propagation, the actual duration in the whole tissue may be longer (approximately 400 ms) than that recorded by a single LFP electrode. Ensemble activity produced a low-amplitude optical signal (7-14% of the interictal-like spikes in the same tissue), suggesting a moderate net depolarization of the population. These were very different from hyperexcitable (epileptiform) events in the same tissue that had about 10 times the optical signal amplitude and propagated at 125 +/- 24 mm/s (n = 21, 6 animals). On a global spatial scale (approximately 0.8 mm wide in layers II-III) ensemble activity had a smooth waveform in voltage-sensitive dye signals (population transmembrane potential). On a local scale, field potential recordings showed large fluctuations with complex oscillations and substantial trial-to-trial variation. This suggests that oscillations in cortical circuits occurred only in small clusters of correlated neurons. Ensemble activity was sensitive to the excitation-inhibition balance of the local network. Antagonists of N-methyl-D-aspartate, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, and GABAa receptors, and muscarinic agonists and other modest manipulations such as increasing bath concentration of Mg(2+) to 2.5-4 mM (normally at 2 mM), or K(+) to 5-7 mM (normally 3 mM), all significantly reduced the probability of evoking the activity. The metabotropic glutamate receptor agonist, aminocyclopentane-1,3-dicarboxylic acid, blocked the activity at a low concentration (10-15 microM), while the antagonist (R,S)-alpha-methyl-4-carboxyphenylglycine had no effect even at high concentration (240 microM). Our data suggest that locally organized neuronal clusters may play a role in the organization of oscillatory activities in the gamma band and may participate in cortical integration/amplification occurring on a scale of approximately 1 mm x 300 ms.

Animals↗
PubMed2001

Comparison of MRI perfusion imaging and single photon emission computed tomography in chronic stroke.

There have been few direct comparisons between MR perfusion-weighted imaging (PWI) and established perfusion imaging techniques, and none in chronic stroke. We therefore studied 17 chronic hemispheric infarction patients (mean, 90 days) and compared hypoperfusion volumes determined from PWI maps of relative cerebral blood flow (rCBF) and volume (rCBV), and mean transit time (rMTT) with those measured with (99)Tc-HMPAO single photon emission computed tomography (SPECT). Comparisons were also made between infarct size (T(2)-WI) and clinical scales. Correlations were found between lesion location and volume in all three PWI hemodynamic parameter maps with clinical state and lesions on SPECT and T(2)-WI. In 3 patients, rCBF and rCBV lesions extended well beyond the borders of moderate-sized infarctions. We conclude that in chronic stroke, PWI can delineate regions of abnormal perfusion that reflect the degree of functional impairment and structural damage. The finding of peri-infarct hypoperfusion suggests that PWI may have the potential to provide a rapid and non-invasive template against which interventional strategies aimed at promoting functional recovery may be investigated.

Aged↗
PubMed2001

Perfusion magnetic resonance imaging maps in hyperacute stroke: relative cerebral blood flow most accurately identifies tissue destined to infarct.

BACKGROUND AND PURPOSE: In ischemic stroke, perfusion-weighted imaging (PWI) and diffusion-weighted imaging (DWI) provide important pathophysiological information. A PWI>DWI mismatch pattern suggests the presence of salvageable tissue. However, improved methods for distinguishing PWI>DWI mismatch tissue that is critically hypoperfused from benign oligemia are required. METHODS: We investigated the usefulness of maps of relative cerebral blood flow (rCBF), volume (rCBV), and mean transit time (rMTT) to predict transition to infarction in hyperacute (<6 hours) stroke patients with PWI>DWI mismatch patterns. Semiquantitative color-thresholded analysis was used to measure hypoperfusion volumes, including increasing color signal intensity thresholds of rMTT delay, which were compared with infarct expansion, outcome infarct size, and clinical status. RESULTS: Acute rCBF lesion volume had the strongest correlation with final infarct size (r=0.91, P<0.001) and clinical outcome (r=0.67, P<0.01). There was a trend for acute rCBF>DWI mismatch volume to overestimate infarct expansion between the acute and outcome study (P=0.06). Infarct expansion was underestimated by acute rCBV>DWI mismatch (P<0.001). When rMTT lesions included tissue with moderately prolonged transit times (mean delay 4.3 seconds, signal intensity values 50% to 70%), infarct expansion was overestimated. In contrast, when rMTT lesions were restricted to more severely prolonged transit times (mean delay 6.1 seconds, signal intensity >70%), these regions progressed to infarction in all except 1 patient, but infarct expansion was underestimated (P<0.001). CONCLUSIONS: The acute rCBF lesion most accurately identified tissue in the PWI>DWI mismatch region at risk of infarction. Color-thresholded PWI maps show potential for use in an acute clinical setting to prospectively predict tissue outcome.

Acute Disease↗
PubMed2001

Vascular endothelial growth factor-mediated endothelium-dependent relaxation is blunted in spontaneously hypertensive rats.

The vasodilatory effect of VEGF has not been characterized in the setting of hypertension. This study investigated the in vitro vasorelaxant effects of VEGF in organ chambers in the aorta of the adult (12-week-old) spontaneously hypertensive rats (SHR), young (4-week-old) SHR without hypertension, and age-matched Wistar-Kyoto (WKY) rats compared with acetylcholine (ACh). Cumulative concentration-relaxation curves were established for VEGF (approximately 10(-12)-10(-8.5) M) and ACh (approximately 10(-10)-10(-5) M) in U46619 (10(-8) M)-induced contraction. VEGF induced endothelium-dependent relaxation that was significantly reduced in the adult SHR compared with the age-matched WKY control (87.8 +/- 2.8 versus 61.4 +/- 8.6%, P = 0.01). These responses were significantly attenuated by pretreatment with N(omega)-nitro-L-arginine (L-NNA, 300 microM) alone (SHR: 25.1 +/- 1.9%; WKY: 21.0 +/- 2.6%; P = 0.01) or indomethacin (7 microM) + L-NNA (SHR: 30.2 +/- 2.1%; WKY: 35.0 +/- 2.9%; P = 0.01). Further addition of oxyhemoglobin (20 microM) abolished the residual relaxation and reduced the relaxation induced by nitroglycerin. ACh induced similar responses to VEGF. In contrast, pretreatment with indomethacin alone enhanced VEGF- or ACh-induced relaxations and the effect was greater in the adult SHR than in WKY rats. In contrast to the adult SHR versus WKY rats, there were no significant differences of VEGF- or ACh-induced relaxations between young SHR and WKY rats. The results demonstrate that VEGF induces endothelium- or nitric oxide-dependent relaxation, which is blunted in the adult SHR. The mechanism of this impairment may be related to decreased release of NO although increased release of contracting factors from the dysfunctional endothelium may also be involved.

Acetylcholine↗
PubMed2001

[Role of protein kinase in the proliferation of human embryonic pulmonary fibrolasts stimulated by the supernatants of crocidolite-exposed alveolar macrophages].

In order to study the role of protein kinase in the proliferation of lung fibroblasts induced by crocidolite. An in vitro model was established by rabbit alveolar macrophage (AM) and human embryonic pulmonary fibroblasts (HEPF). Using MTT color response method to measure HEPF proliferation, the influence of the inhibitor or activator of protein kinase (PKA, PKC and TPK) on the proliferation of crocidolite-induced HEPF were investigated. TiO2 was taken as negative control and SiO2 positive control. The results showed that the inhibitors of PKA, PKC and TPK could all inhibit the proliferation of HEPF induced by crocidolite, their activators could also promote the proliferation of HEPF. There all existed significant dose-effect relationships (P < 0.01), and the intensity in crocidolite group was inhibited or activated more than that in the controls. Through acting intensity analysis, the intensity was found as follows: TPK > PKC > PKA. It was suggested that TPK, PKC and PKA signal pathways were all involved in the process of the proliferation of crocidolite-induced HEPF, but TPK maybe played a key role in this process. This study provide leads for further research on identifying the bioactive factors of proliferation of crocidolite-induce HEPF.

Animals↗
PubMed2001

Scabies associated with radiation therapy for cutaneous T-cell lymphoma.

Scabies, infection with Sarcoptes scabiei, is known to be predisposed to by poor body hygiene, environmental exposure, and systemic immunodeficiency. We report the case of an 83-year-old man with Sezary's syndrome who developed scabies limited to the skin of the upper chest, the same location where he had previously received electron beam radiation treatments for cutaneous T-cell lymphoma. Histologic and immunohistochemical studies demonstrated that sections of the previously irradiated right and left chest skin, compared to non-irradiated chest, abdominal, and leg skin, had infestation by scabies, diminished involvement by T-cell lymphoma, and notably reduced numbers of Langerhans cells. These findings suggest that the development of scabies may be predisposed to by local cutaneous radiation therapy, and that it may be mediated by local cutaneous immunodeficiency secondary to reduced numbers of Langerhans cells.

Aged↗