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Biomedical subjects

W Zhou

Publications and source records attributed to W Zhou.

At least 307 records · Page 17Linked to original sources

Effects of heat production attributable to forced walking on thermoregulatory physiological responses of chickens in a warm environment.

1. To determine the effects of heat production on thermoregulatory physiological responses, 5 chickens were forced to walk to increase heat production. The study consisted of two experiments. One involved 3 walking speeds (8, 16 and 24 m/min) at 25 degrees C ambient temperature. The other involved a single walking speed of 16 m/min at 3 ambient temperatures (20, 25 and 30 degrees C). Heat production, heart rate, abdominal temperature, shank skin temperature and respiration rate were measured before, during and after walking. 2. Heat production, heart rate and respiration rate increased abruptly after the start of walking and with increase in walking speed. At the start of walking, an abrupt increase in abdominal temperature occurred independently of walking speed and environmental temperature; then, as walking continued, abdominal temperature increased further with increasing walking speed and increasing environmental temperature. Shank skin temperature declined at the initiation of walking, then increased. 3. Heat production and heart rate recovered rapidly after walking, while shank skin temperature and respiration rate increased and then recovered, except at 30 degrees C. 4. A proportion, 17% to 35%, of the increased heat production was stored, increasing body temperature during walking. After walking, the stored heat was lost by means of panting until abdominal temperature recovered to 41 degrees C or shank skin temperature recovered to 37 degrees C. 5. These results suggest that the greatly-increased heat production attributable to forced walking leads to abrupt thermoregulatory physiological responses, and the heat stored in the body is actively dissipated by panting until abdominal temperature recovers to the pre-walking level. The chief mode of heat loss of birds changes with deep body temperature.

Animals↗

A dual-function palindromic sequence regulates testis-specific transcription of the mouse lactate dehydrogenase c gene in vitro.

The promoter of the mouse lactate dehydrogenase c (Ldh-c) gene was assayed in an in vitro transcription system. Of the nuclear extracts isolated from several mouse tissues, only testis supported transcription from a 710 Ldh-c promoter fragment. Mutation analysis indicated that a canonical TATA box and a 30-bp palindromic sequence are both required for promoter activity. Liver nuclear extract (LN) can reduce transcriptional activity significantly when added to testis nuclear extract (TN). Deletion of the 3' palindromic sequence resulted in a low level of transcriptional activity in LN. Competition with a double-stranded synthetic palindromic oligonucleotide inhibited transcription in TN and rescued a low level of transcription in LN. Our results strongly indicate that the palindromic sequence contains both a negative element for repression in somatic tissues and a positive element for activation of the Ldh-c gene in testis.

Animals↗

Autoradiographic localization of cholecystokinin (CCK) receptor expression during the development of azaserine-induced rat pancreatic carcinoma.

The peptide hormone cholecystokinin (CCK) has been shown to stimulate the growth of azaserine-induced preneoplastic nodules in the rat pancreas. Previously, our labortory demonstrated by classical binding studies that CCK receptors are overexpressed in azaserine-induced rat pancreatic neoplasms. In the present study, we utilized autoradiography to determine the temporal course of this increased receptor binding. Male Lewis rats were given azaserine or saline injections and sacrificed at 2, 4, 8, 12, and 18 months of age. Pancreatic tissue was harvested and autoradiography using 125l-labeled. CCK-8 was performed. Densitometry measurements of azaserine-induced pancreatic nodules, internodular pancreas, and normal pancreatic tissue (from saline-treated controls) of each age group were taken with an image analyzer. There was no statistically significant difference in CCK binding to internodular pancreas and normal pancreas at any age. At 2 months of age, there was no significant increase in CCK binding to azaserine-induced pancreatic nodules. However, at 4, 8, 12, and 18 months of age there was significantly greater CCK binding to azaserine-induced pancreatic nodules than to both internodular pancreas and normal pancreas (p < 0.001 for all groups). At 18 months of age, one azaserine-treated animal developed a pancreatic acinar cell carcinoma, which likewise exhibited significantly greater CCK binding than internodular pancreas or normal pancreas (p < 0.001 for both). These findings demonstrate increased CCK binding in azaserine-induced preneoplastic pancreatic nodules and pancreatic acinar cell carcinoma, compatible with our previous demonstration of receptor overexpression in these tissues. Increased CCK binding first becomes apparent by 4 months following exposure to azaserine. These result suggest that overexpression of CCK receptors, located specifically on preneoplastic and neoplastic pancreatic lesions, results in increased CCK binding and is involved in the mediation of CCK-stimulated growth during azaserine-induced pancreatic carcinogenesis.

Animals↗

Differential membrane binding of the human immunodeficiency virus type 1 matrix protein.

The human immunodeficiency virus type 1 matrix protein (p17MA) plays a central role at both the early and late stages of the virus life cycle. During viral assembly, the p17MA domain of Pr55gag promotes membrane association, which is essential for the formation of viral particles. When viral infection occurs, the mature p17MA dissociates from the plasma membrane and participates in the nuclear targeting process. Thus, p17MA contains a reversible membrane binding signal to govern its differential subcellular localization and biological functions. We previously identified a membrane binding signal within the amino-terminal 31 amino acids of the matrix domain of human immunodeficiency virus type 1 Gag, consisting of myristate and a highly basic region (W. Zhou, L. J. Parent, J. W. Wills, and M. D. Resh, J. Virol. 68:2556-2569, 1994). Here we show that exposure of this membrane binding signal is regulated in different Gag protein contexts. Within full-length Pr55gag, the membrane targeting signal is exposed and can direct Pr55gag as well as heterologous proteins to the plasma membrane. However, in the context of p17MA alone, this signal is hidden and unable to confer plasma membrane binding. To investigate the molecular mechanism for regulation of membrane binding, a series of deletions within p17MA was generated by sequentially removing alpha-helical regions defined by the nuclear magnetic resonance structure. Removal of the last alpha helix (amino acids 97 to 109) of p17MA was associated with enhancement of binding to biological membranes in vitro and in vivo. Liposome binding experiments indicated that the C-terminal region of p17MA exerts a negative effect on the N-terminal MA membrane targeting domain by sequestering the myristate signal. We propose that mature p17MA adopts a conformation different from that of the p17MA domain within Pr55gag and present evidence to support this hypothesis. It is likely that such a conformational change results in an N-terminal myristyl switch which governs differential membrane binding.

Animals↗

E2F-1 blocks terminal differentiation and causes proliferation in transgenic megakaryocytes.

The transcription factor E2F-1 plays a central role in the cell cycle through its ability to activate genes involved in cell division. E2F-1 activity is regulated by a number of proteins, including the retinoblastoma susceptibility gene product, cyclin-dependent kinases, and their inhibitors, proteins that have been implicated in the control of certain developmental processes. To investigate a potential role of E2F-1 in differentiation, we assayed the ability of megakaryocytes to form platelets in an in vivo transgenic model. E2F-1 expression in megakaryocytes blocked differentiation during maturation, resulting in severe thrombocytopenia. Ultrastructural analysis of megakaryocytes revealed abnormal development characterized by hyperdemarcation of cytoplasmic membranes and reduced numbers of alpha granules. Administration of megakaryocyte growth and development factor or interleukin 6 could not overcome the differentiation block. Additionally, E2F-1 caused massive megakaryocyte accumulation in both normal and ectopic sites, first evident in E15 embryonic liver. Furthermore, significant apoptosis was observed in transgenic megakaryocytes. These data indicate that E2F-1 can prevent terminal differentiation, probably through its cell cycle-stimulatory activity.

Animals↗

Regulation of AE2 Cl-/HCO3- exchanger during intestinal development.

The Na(+)-independent Cl-/HCO3- exchangers in many tissues are encoded by AE2, which is a member of the anion-exchanger (AE) gene family. Molecular regulation of AE2 remains mostly unknown. In this study, AE2 mRNA levels during enterocyte differentiation and intestinal development were examined in rat small intestines. AE2 mRNA levels did not show obvious segmental variation or vary along the crypt-villus axis. In contrast, AE2 mRNA decreased between days 14 and 21 after birth, the period corresponding to the transition period between the suckling and weanling stages in rats. Effects of L-thyroxine and dexamethasone on AE2 expression were examined because these hormones play important roles in gene regulation during development. L-Thyroxine administration starting on day 9 after birth led to an approximately 60% decrease (P < 0.001) in AE2 mRNA on day 13. Dexamethasone had no effect on AE2 mRNA level regardless of whether the hormone was administered alone or in conjunction with L-thyroxine. Our results indicate that AE2 mRNA in the intestine is regulated during development and that this regulation may in part be related to hormonal changes.

Aging↗

Complement synthesis in the injured kidney: does it have a role in immune complex glomerulonephritis?

On pages 2428 to 2433 of this issue, Miyazaki et al. provide evidence that complement component C3 is synthesized within the glomeruli of patients with mesangial glomerulonephritis. Although it has been known for several years that cells isolated from the human kidney can synthesize a range of complement components, and that immune complex disease can increase the expression of these genes, it is only now that the link between intraglomerular synthesis of complement and human glomerulonephritis can be made. In view of the long interest in the role of complement in the pathogenesis of glomerulonephritis, this begs the question to what extent local complement synthesis may be involved in the generation of tissue injury. Given also the double-sided nature of complement-proinflammatory and protective-It remains to be seen if the roles of local and systemic complement differ in these respects. To weigh these questions, we examine the current evidence that connects local complement synthesis with renal injury, and ask what studies are needed to provide more definitive answers.

Animals↗

Effectiveness of a zinc amino acid chelate and zinc sulfate in restoring serum and soft tissue zinc concentrations when fed to zinc-depleted pigs.

In a 36-d experiment, 32 pigs were depleted of Zn (24 d) using a soy-isolate (basal) diet (17 mg/kg of Zn) and then fed the basal diet (12 d) supplemented with 45 mg/kg of Zn from ZnSO4 (purified zinc sulfate dry powder, ZnSO4.nH2O) or from a Zn amino acid chelate (ZnAAC) to study the effectiveness of these dietary Zn sources in restoring serum and soft tissue Zn concentrations. Concurrently, nondepleted pigs were pair-fed both Zn-supplemented diets (eight pigs per diet) throughout the experiment. Serum Zn concentrations and serum alkaline phosphatase (ALP) activity of pigs fed the diets with no supplemental Zn were lower (P < .05) than those of nondepleted pigs after 7 and 14 d, respectively. After 24 d, concentrations of Zn in liver, pancreas, kidney, brain, and small intestine of Zn-depleted pigs were lower (P < .01) than those of nondepleted pigs. Except for decreased (P < .001) kidney Cu, soft tissue Cu and Fe concentrations were not affected by Zn status or Zn source. From d 24 to 36 (Zn repletion), serum and tissue Zn concentrations and serum ALP activities increased (P < .05), but the response was similar for both Zn sources in Zn-depleted and nondepleted pigs. At d 30 and 36, kidney Cu was increased (P < .01) in Zn-depleted pigs fed 45 mg/kg of Zn as either ZnSO4 or ZnAAC. Furthermore, Fe concentration was higher (P < .05) in intestinal segments of Zn-depleted and nondepleted pigs fed ZnAAC than in pigs fed ZnSO4. Accumulations of Cu in the kidney and Fe in the small intestine were affected by depletion and repletion of Zn and by dietary Zn source, respectively. In conclusion, serum and soft tissue Zn concentrations were clearly affected by Zn status: however, an effect of Zn source was not observed.

Alkaline Phosphatase↗

[The application of Ultrasound Biomicroscope in anterior segment contusion].

PURPOSE: To study the clinical value of Ultrasound Biomicroscope in anterior segment contusion. METHODS: Seven eyes with anterior segment contusion were examined by regular ophthalmic examination, ophthalmic B-scan, and Ultrasound Biomicroscope. RESULTS: Ultrasound Biomicroscope can show angle recession, cyclodialysis, iridodialysis, zonular breaking, lens dislocation and vitreous protrusion to posterior chamber. In most cases cyclodialysis and shallow detachment of choroid can not be diagnosed because shallow anterior chamber and hypton. CONCLUSION: The result suggests that Ultrasound Biomicroscope has high clinical value in diagnosis of anterior segment contusion, especially in cornea edema, hyphemia, hypton, Ultrasound Biomicroscope can refer precise diagnosis of anterior segment contusion.

Adult↗

A scanning electron microscopic study of trabeculae in osteoporotic femoral head.

OBJECTIVE: To investigate osteoclastic resorption in trabeculae of osteoporotic femoral head. METHODS: Osteoporotic femoral heads were collected from 7 aged women with an average age of 72.4 years, who underwent endoprosthetic replacement for intracapsular hip fracture. Femoral head trabeculae from 3 young adults killed in traffic accidents served as control. The two types of specimens were processed and studied under scanning electron microscope. RESULTS: The trabeculae of femoral head formed round or roundish arch structure. The columnar trabeculae of femoral head in the aged women showed overt osteoclastic resorption, manifested in thinning, tapering and perforation, resulting in formation of icicle-like trabeculae, which then became rounded, lost height and eventually turned into small tubercle. As a result, the inter-trabecular space enlarged markedly. Under high magnification, the trabeculae could be discerned oval, narrow oval or spindle-shaped. Howship resorption lacunae, which varied in size, depth and content, but all revealed punched-out margin. During bone resorption, the inorganic and organic components were successively resorbed. In the Howship lacunae and surrounding areas, newly formed collagen fibrils and bone tissues emerged, signifying reversal and new bone formation phases after bone resorption phase. CONCLUSION: Osteoclastic resorption markedly compromises the structural integrity and strength of the trabeculae of the arch structure of the femoral head in the aged women.

Age Factors↗

[Induced-expression of MHC-DR molecules on mice islet cells].

The correlation of induced-expression of MHC-DR molecules with insulin release in cultured mice islet cells has been studied. The results showed that, (1) No detectable induced-expression of MHC-DR molecules by TNF-alpha alone at the concentration of 50-100 U/ml has been assayed, but the induced-expression of MHC-DR molecules has been identified in a few islet cells (8.5 +/- 2.9%) with IFN-r alone at concentration of 50-100 U/ml. (2) The induced-expression of MHC-DR molecules has been detected in as high as 80% of cultured islet cells with TNF-alpha and IFN-r combined at different concentrations. (3) Insulin released from cultured islet cells was enhanced by IFN-r and TNF-alpha either alone or combined at different concentrations. These results suggest that the induced-expression of MHC-DR molecules themselves does not damage the function for insulin release in cultured islet cells.

Animals↗

Endoscopic Intranasal dacryocystorhinostomy in forty-five patients.

OBJECTIVE: To observe the results of endoscopic intranasal dacryocystorhinostomy. METHODS: Forty-five patients (forty-eight eyes) suffering from chronic dacryocystitis received endoscopic intranasal dacryocystorhinostomy after November 1991, and were followed up for 3 to 36 months. RESULTS: Thirty-nine eyes were cured (81.2%). It is significantly effective (8.3%) in 4 eyes, and effective in 2 eyes (4.2%). The total effective rate was 93.7%. CONCLUSIONS: The intranasal approach is simple causing little bleeding and no facial scar. With the self-made dacryocyst-illuminator (diameter = 0.8 mm), and by transilluminating the lacrimal sac with fiberoptic intraocular endoilluminator bundle, the sac can be located endonasally, thus facilitating the approach.

Adult↗

[Nucleotide sequence of HLA-DQA1 promoter region (QAP) in a lung cancer patient].

The HLA-DQA1 allele and nucleotide sequence of HLA-DQA1 promoter region (QAP) in a patient with IDDM complicated lung cancer have been identified by PCR/SSCP, PCR/SSCP and PCR/sequencing. The results showed that: (1) All of the lung cancer patient and his family members carried HLA-DQA1* 0301/0501 alleles. (2) a single base substitution G-->A at position -155 and deletion CAA at position -161 to -163 occurred in the patient. These results suggest that the mutation of HLA-DQA1 promoter region may modulate HLA-DQA1 gene expression by trans-acting factors binding to variant cis-acting elements and may be responsible for pathogenesis of lung cancer.

Alleles↗

[A study of high-pass resolution perimetry in the early diagnosis of primary open-angle glaucoma].

OBJECTIVE: To evaluate the application of high-pass resolution perimetry (HRP) in detecting the early visual field loss of glaucoma. METHOD: According to the method described by Frisén, we developed HRP in a personal computer. The HRP was used to examine the visual field of 22 normal subjects (44 eyes), 27 cases (41 eyes) of primary open-angle glaucoma (POAG) with abnormal automated visual fields and 10 cases (13 eyes) of early POAG or suspected POAG with normal automated visual fields. RESULTS: The mean resolution threshold in the normal subjects was 3.96+/- 0.55db in the right eyes and 3.98+/- 0.55dB in the left eyes. It is demonstrated that HRP was more sensitive than automated perimetry in detecting the glaucomatous visual field defects, its sensitivity was 93.75% and specificity was 97.7%. The early visual field loss of glaucoma might present increment of the retinal resolution threshold. CONCLUSION: HRP is a relatively sensitive method for the detection of the early visual field loss in POAG, and it can be used extensively.

Adult↗

T7 RNA polymerase bypass of large gaps on the template strand reveals a critical role of the nontemplate strand in elongation.

We show that T7 RNA polymerase can efficiently transcribe DNA containing gaps from one to five bases in the template strand. Surprisingly, broken template strands missing up to 24 bases can still be transcribed, although at reduced efficiency. The resulting transcripts contain the full template sequence with the RNA deleted for the gapped region missing on the template strand. These findings indicate that the end of a downstream template strand can be brought into the polymerase and transcribed as if it were a part of an intact polynucleotide chain by utilizing the unpaired nontemplate strand. This, as well as transcription of an intact template strand, relies heavily upon the non-template strand, suggesting that a duplex DNA-binding site on the leading edge of RNA polymerase is required for RNA chain elongation on DNA templates. This work contributes substantially to the emerging picture that the nontemplate strand is an important element of the transcription elongation complex.

Bacteriophage T7↗

A locus of the gonadotropin-releasing hormone receptor that differentiates agonist and antagonist binding sites.

The decapeptide gonadotropin-releasing hormone controls reproductive function via interaction with a heptahelical G protein-coupled receptor. Because of molecular model of the receptor predicts that Lys121 in the third transmembrane helix contributes to the binding pocket, the function of this side chain was studied by site-directed mutagenesis. Substitution of Arg at this position preserved high affinity agonist binding, whereas Gln at this position reduced binding below the limits of detection. Leu and Asp at this locus abolished both binding and detectable signal transduction. The EC50 of concentration-response curves for coupling to phosphatidyl inositol hydrolysis obtained with the Gln121 receptor was more than 3 orders of magnitude higher than that obtained for the wild-type receptor. In order to determine whether the increased EC50 obtained with this mutant reflects an altered receptor affinity, the effect of decreases in wild-type receptor density on concentration-response curves was determined by irreversible antagonism. Progressively decreasing the concentration of the wild-type receptor increased the EC50 values obtained to a maximal level of 2.4 +/- 0.2 nM. Comparison of this value with the EC50 of 282 +/- 52 nM observed with the Gln121 receptor mutant indicates that the agonist affinity for this mutant is reduced more than 100-fold. In contrast, antagonist had comparable high affinities for the wild-type, Arg121, and Gln121 mutants. The results indicate that a charge-strengthened hydrogen bond donor is required at this locus for high affinity agonist binding but not for high affinity antagonist binding.

Amino Acid Sequence↗