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M Z Zhang

Publications and source records attributed to M Z Zhang.

At least 19 recordsLinked to original sources
PubMed2001

Genetic deletion of COX-2 prevents increased renin expression in response to ACE inhibition.

Cyclooxygenase-2 (COX-2) is expressed in macula densa (MD) and surrounding cortical thick ascending limb of the loop of Henle (cTALH) and is involved in regulation of renin production. We and others have previously found that selective COX-2 inhibitors can inhibit renal renin production (Cheng HF, Wang JL, Zhang MZ, Miyazaki Y, Ichikawa I, McKanna JA, and Harris RC. J Clin Invest 103: 953-961, 1999; Harding P, Sigmon DH, Alfie ME, Huang PL, Fishman MC, Beierwaltes WH, and Carretero OA. Hypertension 29: 297-302, 1997; Traynor TR, Smart A, Briggs JP, and Schnermann J. Am J Physiol Renal Physiol 277: F706-F710, 1999; Wang JL, Cheng HF, and Harris RC. Hypertension 34: 96-101, 1999). In the present studies, we utilized mice with genetic deletions of the COX-2 gene in order to investigate further the potential role of COX-2 in mediation of the renin-angiotensin system (RAS). Age-matched wild-type (+/+), heterozygotes (+/-), and homozygous null mice (-/-) were administered the angiotensin-converting enzyme inhibitor (ACEI), captopril, for 7 days. ACEI failed to significantly increase plasma renin activity, renal renin mRNA expression, and renal renin activity in (-/-) mice. ACEI increased the number of cells expressing immunoreactive renin in the (+/+) mice both by inducing more juxtaglomerular cells to express immunoreactive renin and by recruiting additional renin-expressing cells in the more proximal afferent arteriole. In contrast, there was minimal recruitment of renin-expressing cells in the more proximal afferent arteriole of the -/- mice. In summary, these results indicate that ACEI-mediated increases in renal renin production were defective in COX-2 knockout (K/O) mice and provide further indication that MD COX-2 is an important mediator of the renin-angiotensin system.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Boron neutron capture therapy of brain tumors: biodistribution, pharmacokinetics, and radiation dosimetry sodium borocaptate in patients with gliomas.

OBJECTIVE: The purpose of this study was to obtain tumor and normal brain tissue biodistribution data and pharmacokinetic profiles for sodium borocaptate (Na2B12H11SH) (BSH), a drug that has been used clinically in Europe and Japan for boron neutron capture therapy of brain tumors. The study was performed with a group of 25 patients who had preoperative diagnoses of either glioblastoma multiforme (GBM) or anaplastic astrocytoma (AA) and were candidates for debulking surgery. Nineteen of these patients were subsequently shown to have histopathologically confirmed diagnoses of GBM or AA, and they constituted the study population. METHODS: BSH (non-10B-enriched) was infused intravenously, in a 1-hour period, at doses of 15, 25, and 50 mg boron/kg body weight (corresponding to 26.5, 44.1, and 88.2 mg BSH/kg body weight, respectively) to groups of 3, 3, and 13 patients, respectively. Multiple samples of tumor tissue, brain tissue around the tumors, and normal brain tissue were obtained at either 3 to 7 or 13 to 15 hours after infusion. Blood samples for pharmacokinetic studies were obtained at times up to 120 hours after termination of the infusion. Sixteen of the patients underwent surgery at the Beijing Neurosurgical Institute and three at The Ohio State University, where all tissue samples were subsequently analyzed for boron content by direct current plasma-atomic emission spectroscopy. RESULTS: Blood boron values peaked at the end of the infusion and then decreased triexponentially during the 120-hour sampling period. At 6 hours after termination of the infusion, these values had decreased to 20.8, 29.1, and 62.6 microg/ml for boron doses of 15, 25, and 50 mg/kg body weight, respectively. For a boron dose of 50 mg/kg body weight, the maximum (mean +/- standard deviation) solid tumor boron values at 3 to 7 hours after infusion were 17.1+/-5.8 and 17.3+/-10.1 microg/g for GBMs and AAs, respectively, and the mean tumor value averaged across all samples was 11.9 microg/g for both GBMs and AAs. In contrast, the mean normal brain tissue values, averaged across all samples, were 4.6+/-5.1 and 5.5+/-3.9 microg/g and the tumor/normal brain tissue ratios were3.8 and 3.2 for patients with GBMs and AAs, respectively. The large standard deviations indicated significant heterogeneity in uptake in both tumor and normal brain tissue. Regions histopathologically classified either as a mixture of tumor and normal brain tissue or as infiltrating tumor exhibited slightly lower boron concentrations than those designated as solid tumor. After a dose of 50 mg/kg body weight, boron concentrations in blood decreased from 104 microg/ml at 2 hours to 63 microg/ml at 6 hours and concentrations in skin and muscle were 43.1 and 39.2 microg/g, respectively, during the 3- to 7-hour sampling period. CONCLUSION: When tumor, blood, and normal tissue boron concentrations were taken into account, the most favorable tumor uptake data were obtained with a boron dose of 25 mg/kg body weight, 3 to 7 hours after termination of the infusion. Although blood boron levels were high, normal brain tissue boron levels were almost always lower than tumor levels. However, tumor boron concentrations were less than those necessary for boron neutron capture therapy, and there was significant intratumoral and interpatient variability in the uptake of BSH, which would make estimation of the radiation dose delivered to the tumor very difficult. It is unlikely that intravenous administration of a single dose of BSH would result in therapeutically useful levels of boron. However, combining BSH with boronophenylalanine, the other compound that has been used clinically, and optimizing their delivery could increase tumor boron uptake and potentially improve the efficacy of boron neutron capture therapy.

Adult↗
PubMed2000

Nitric oxide regulates renal cortical cyclooxygenase-2 expression.

We have previously shown that cyclooxygenase-2 (COX-2) is localized to the cortical thick ascending limb of the loop of Henle (cTALH)/macula densa of the rat kidney, and expression increases in response to low-salt diet and/or angiotensin-converting enzyme (ACE) inhibition. Because of the localization of neuronal nitric oxide synthase (nNOS) to macula densa and surrounding cTALH, the present study investigated the role of nitric oxide (NO) in the regulation of COX-2 expression. For in vivo studies, rats were fed a normal diet, low-salt diet or low-salt diet combined with the ACE inhibitor captopril. In each group, one-half of them were treated with the nNOS inhibitors 7-nitroinidazole (7-NI) or S-methyl-thiocitrulline. Both of these NOS inhibitors inhibited increases in COX-2 mRNA and immunoreactive protein in response to low salt and low salt+captopril. For in vitro studies, COX-2 expression was studied in primary cultures of rabbit cTALH cells immunodisssected with Tamm-Horsfall antibody. Basal COX-2 immunoreactivity expression was stimulated by S-nitroso-N-acetyl-penicillamine (SNAP), an NO donor, and intracellular cGMP concentration. The cultured cells expressed immunoreactive nNOS, and 7-NI inhibited basal COX-2 immunoreactivity expression, which could be partially overcome by cGMP. In summary, these studies indicate that NO is a mediator of increased renal cortical COX-2 expression seen in volume depletion and suggest important interactions between the NO and COX-2 systems in the regulation of arteriolar tone and the renin-angiotensin system by the macula densa.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Role of p38 in the regulation of renal cortical cyclooxygenase-2 expression by extracellular chloride.

We have previously shown that in renal cortex, COX-2 expression is localized to macula densa and surrounding cortical thick ascending limb of Henle (cTALH). Dietary salt restriction increases local expression of COX-2, which mediates renin production and secretion. Given that decreased luminal chloride [Cl(-)] at the level of the macula densa increases renin production and secretion, we investigated the role of extracellular ion concentration on COX-2 expression. Quiescent rabbit cTALH cells were incubated in a physiological salt solution containing high or low levels of NaCl. Immunoreactive COX-2 expression increased significantly in the low NaCl solution. COX-2 expression also increased after administration of the Na(+)/K(+)/2Cl(-) cotransport inhibitor, bumetanide. Selective substitution of chloride led to increased COX-2 expression, whereas selective substitution of sodium had no effect. The p38 MAP kinase inhibitor PD169316 decreased low NaCl-induced COX-2 expression. Low-salt or low-chloride medium induced cultured cTALH to accumulate >/= 3-fold higher levels of pp38, the activated (phosphorylated) form of p38; low-salt medium also increased pJNK and pERK levels. Feeding rats a low-salt diet for 14 days induced a significant increase in renal cortical pp38 expression, predominantly in the macula densa and cTALH. These results suggest that reduced extracellular chloride leads to increased COX-2 expression, which may be mediated by activation of a p38-dependent signaling pathway.

Animals↗
PubMed1999

Regulation of cyclooxygenase-2 (COX-2) in rat renal cortex by adrenal glucocorticoids and mineralocorticoids.

Production of prostaglandins involved in renal salt and water homeostasis is modulated by regulated expression of the inducible form of cyclooxygenase-2 (COX-2) at restricted sites in the rat renal cortex. Because inflammatory COX-2 is suppressed by glucocorticoids, and prostaglandin levels in the kidney are sensitive to steroids, the sensitivity of COX expression to adrenalectomy (ADX) was investigated. By 2 weeks after ADX in mature rats, cortical COX-2 immunoreactivity increased 10-fold in the cortical thick ascending limb and macula densa. The constitutive isoform, COX-1, was unchanged. The magnitude of the changes and specificity of COX-2 immunoreactivity were validated by in situ hybridization histochemistry of COX-2 mRNA and Western blot analysis. Increased COX-2 activity (>5-fold) was documented by using a specific COX-2 inhibitor. The COX-2 up-regulation in ADX rats was reversed by replacement therapy with either corticosterone or deoxycorticosterone acetate. In normal rats, inhibition of glucocorticoid receptors with RU486 or mineralocorticoid receptors with spironolactone caused up-regulation of renal cortical COX-2. These results indicate that COX-2 expression in situ is tonically inhibited by adrenal steroids, and COX-2 is regulated by mineralocorticoids as well as glucocorticoids.

Adrenalectomy↗
PubMed1999

Angiotensin II attenuates renal cortical cyclooxygenase-2 expression.

We have previously shown that in rat renal cortex, cyclooxygenase-2 (COX-2) expression is localized to cTALH cells in the region of the macula densa, and that dietary salt restriction increases COX-2 expression. Administration of the angiotensin converting inhibitor, captopril, further increased COX-2 mRNA and renal cortical COX-2 immunoreactivity, with the most pronounced expression in the macula densa. Administration of an AT1 receptor antagonist, losartan, also significantly increased cortical COX-2 mRNA expression and COX-2 immunoreactivity. Mutant mice homozygous for both Agtr1a and Agtr1b null mutations (Agtr1a-/-,Agtr1b-/-) demonstrated large increases in immunoreactive COX-2 expression inthe cTALH/macula densa. To determine whether increased COX-2expression in response to ACE inhibition mediated increases in renin production, rats were treated with captopril for one week with or without the specific COX-2 inhibitor, SC58236. Plasma renin activity increased significantly in the captropril group, and this increase was significantly inhibited by simultaneous treatment with SC58236. Thus, these studies indicated that angiotensin II inhibitors augment upregulation of renal cortical COX-2 in states of volume depletion, suggesting that negative feedback by the renin-angiotensin system modulates renal cortical COX-2 expression and that COX-2 is a mediator of increased renin production in response to inhibition of angiotension II production.

Angiotensin II↗
PubMed1998

Prostaglandins in macula densa function.

Cyclooxygenase (COX)-2 mRNA and immunoreactive protein localize to the macula densa and adjacent cortical thick ascending limb in renal cortex, and chronic NaCl restriction increases expression of this enzyme. These findings suggest an integral role for eicosanoids generated by macula densa-associated COX-2 in mediating renin release. As selective inhibitors of COX-2 become available, it will be important to assess their effects on the renin-angiotensin system and glomerular hemodynamics.

Animals↗
PubMed1998

Constitutive expression of cyclooxygenase-2 in rat vas deferens.

Prostaglandins, lipoid substances discovered in human semen as modulators of uterine muscle contractility, are known to play significant roles in virtually all mammalian organ systems, but their male reproductive functions are unclear. Cyclooxygenase, the rate-limiting enzyme in prostaglandin synthesis, occurs in two isoforms distinguished on the basis of constitutive (COX-1) or inducible (COX-2) expression patterns in mammalian tissues. However, in the adult rat male reproductive system, immunohistochemistry and Western and Northern analysis showed that COX-2 is the predominant isoform and is heavily localized to the epithelium of the distal vas deferens, where constitutive expression is manyfold greater than in any other organs of the body. COX-2 is not detected in the proximal one-half of the vas nor in the testis, epididymis, seminal vesicles, or prostate. Elimination of luminal sperm by vasectomy does not affect COX-2 levels, whereas castration severely depletes COX-2 and androgen replacement after castration restores COX-2, indicating that COX-2 expression in the vas is androgen dependent. Because the distal vas also comprises an extensive submucosal venous plexus connected to the penile corpora cavernosa, prostaglandins from the vas may play a role in erection.

Animals↗
PubMed1998

Selective increase of cyclooxygenase-2 expression in a model of renal ablation.

Previous studies have suggested a possible role for prostaglandins (PGs) in mediating alterations in nephron structure and function ensuing after renal ablation. Two isoforms of cyclooxygenase (COX) have been described: constitutive (COX-1) and inducible (COX-2). We examined expression of these isoforms following subtotal renal ablation (5/6 ablation, RA) in rats. In renal cortex, COX-2 mRNA and immunoreactive protein (IP) increased progressively compared with sham-operated littermates. In contrast, there were no significant changes in COX-1 mRNA expression. In normal kidney, cortical COX-1 IP was immunolocalized predominantly to mesangial cells and collecting tubules, whereas COX-2 IP was found in a subset of cortical thick ascending limb of Henle's loop (CTAL) cells in the region of the macula densa (MD). Following RA, significantly increased COX-2 IP was detected in the MD and surrounding CTAL cells. In addition, fainter immunoreactive COX-2 was detected in scattered visceral epithelial cells and mesangial cells of the glomerulus. Immunoblotting of isolated glomeruli demonstrated a selective increase of glomerular immunoreactive COX-2 expression following RA. No change of COX-1 expression was seen. To determine COX activity, isolated glomeruli were incubated with arachidonic acid and PGE2 measured by enzyme immunoassay (EIA). Compared with sham, glomeruli from 2 wk RA produced significantly more PGs. SC-58560, a selective COX-1 inhibitor, did not inhibit PG production in the remnant glomeruli at concentrations up to 10(-4) M, whereas SC-58236, a relatively selective COX-2 inhibitor, significantly inhibited PG production by RA glomeruli. In preliminary studies, to define mechanisms of altered expression of glomerular COX-2, rat mesangial cells were incubated with serum from sham or 2 wk RA. There were significant increases in COX-2 expression in response to 2 wk RA serum. In summary, these results indicate selective increases in renal cortical COX-2 expression following renal ablation.

Analysis of Variance↗
PubMed1997

Gliogenesis in postnatal rat optic nerve: LC1 + microglia and S100-beta + astrocytes.

Lipocortin 1 (LC1) and S100-beta, two Ca(2+)-binding proteins that serve as specific markers for microglia and astrocytes, respectively, have been used to study postnatal gliogenesis in the rat optic nerve. Computerized image analysis was used to quantify and map the stained and unstained glia in transverse sections (10 microns thick) taken 1-2 mm from the chiasm in optic nerves from rat pups at postnatal day 0 (P0), P7, P14, P21, P28, P38 and adults. The number of astrocytes was remarkably constant (100 per section) at all ages. Because the area of the nerve increases 10-fold from P0 to adult, the population density of astrocytes begins al > 5000 mm-2 and drops to 400 mm-2 in the mature nerve; however, because the nerve length increases two-fold, the number of astrocytes doubles over the same period. In contrast, the number of LC1 + cells per section initially is sparse (4 at P0), increases rapidly up to 36 at P21 and levels off at 49 in adults. The microglia population density is relatively stable throughout development (200-300 mm-2) except during the peak of oligodendroblast apoptosis (P21) when it rises to 450 mm-2. Neonatally, LC1 immunoreactivity predominantly labels spherical-ameboid cells; but by P28 they are replaced by mature ramified microglia. The number of unstained cells (putative oligodendrocytes) per section increases from 11 at P0 to a peak of 308 at P21, and declines slightly to 269 in adults. While generally confirming concepts of astrocyte and oligodendrocyte ontogeny from the literature, the present report adds considerable detail regarding microglia, which often have been ignored. Microglia identified by LC1 immunoreactivity comprise 12% of the glia in adult optic nerve near the chiasm.

Animals↗
PubMed1997

Infraorbital nerve transection and whisker follicle removal in adult rats affect microglia and astrocytes in the trigeminal brainstem. A study with lipocortin1- and S100beta-immunohistochemistry.

Transections of the infraorbital nerve in adult rats resulted in progressive alterations of microglia identified by Lipocortinl immunoreactivity at the sites where the primary afferents terminate, i.e. in the trigeminal brainstem sensory nuclei. Microglia proliferated three- to four-fold. Their cell bodies enlarged and their processes thickened. Microglial responses were similar to the removal of whisker follicles. However, they were restricted to discrete nuclear subregions that matched with the known whisker somatotopy. Astrocytes identified by S100beta immunoreactivity showed minor increases in size and in population density. No microglial or astrocytic reactions were found in the second and third synaptic relays of the somatosensory pathway. Because both types of lesion reportedly lead to the reorganization of primary afferents, our results establish the two experimental designs as valuable tools to elucidate the role of microglia and Lipocortin1 in adult brain plasticity.

Animals↗
PubMed1997

A comparison of the sensitivity of the InPouch TV, Diamond's and Trichosel media for detection of Trichomonas vaginalis.

OBJECTIVE: This study compared the ability of three culture media (InPouch TV, Diamond's, and Trichosel) to support the growth of clinical isolates of Trichomonas vaginalis and their relative sensitivity for detection of the organism. METHODS: The majority of the clinical isolates were obtained from two San Francisco Bay Area clinics. T vaginalis was subcultured in 4 ml of one of the InPouch, Diamond's, or Trichosel media for 24-48 hours before evaluation. Twenty isolates were initially cultured in the InPouch test, 13 with Diamond's, and 10 with Trichosel. A haemocytometer was used to measure the initial concentrations of the organisms. Then serial dilutions were made in saline to yield approximately 2.0 x 10(4), 2.0 x 10(3), and 2.0 x 10(2) motile T vaginalis per ml. A 30 microliter inoculum from each dilution was transferred into 4 ml aliquots of the three media (387 individual tests, 43 x 3 dilutions x 3 media). Microscopic examinations for viable trichomonads were made at 24, 48, and 96 hours. Microscopy was through the pouch wall for the InPouch medium, and through a cover slipped slide with one drop of Diamond's and Trichosel media. RESULTS: At 24 hours, the InPouch demonstrated 84/129 positive, Diamond's 23/129, and Trichosel 18/129. At 48 hours, an accumulative positive rate for the InPouch was 98/129, for Diamond's 55/129, and Trichosel 47/129. At 96 hours the total positives for each test were 112/129 for the InPouch, 78/129 for Diamond's, and 74/129 for Trichosel. CONCLUSIONS: The InPouch TV test was significantly more sensitive than either Diamond's or Trichosel (at 0.01 level of significance, pInPouch > pDiamond's; pInPouch > pTrichosel on all three dilutions at 24, 48, and 96 hours). This increased sensitivity was the result of either a reduced generation time or the larger volume of media examined microscopically.

Animals↗
PubMed1997

Cyclooxygenase-2 in rat nephron development.

The inducible second isoform of cyclooxygenase (COX-2) that mediates inflammation also is expressed at low levels in normal adult rat kidneys and is upregulated in response to noninflammatory stimuli (R. C. Harris, J. A. McKanna, Y. Akai, H. R. Jacobson, R. N. DuBois, and M. D. Breyer, J. Clin. Invest. 94: 2504-2510, 1994). Roles in morphogenesis are indicated by reported teratogenicity of COX inhibitors and renal dysgenesis in COX-2 knockout mice (J. E. Dinchuk, B. D. Car, R. J. Focht, J. J. Johnston, B. D. Jaffee, M. B. Covington, N. R. Contel, V. M. Eng, R. J. Collins, P. M. Czerniak, A. G. Stewart, and J. M. Trzaskos, Nature 378: 406-409, 1995; S. G. Morham, R. Lagenbach, C. D. Loftin, H. F. Tiano, N. Vouloumanos, J. C. Jennette, J. F. Mahler, K. D. Kluckman, A. Ledford, C. A. Lee, and O. Smithies. Cell 83: 473-482, 1995). Blots from developing rat kidneys demonstrated that COX-2 mRNA and immunoreactive protein were present in neonates, peaked in the 2nd and 3rd postnatal weeks and declined to adult levels by the 3rd month. Immunolocalization and in situ hybridization detected intense COX-2 immunoreactivity and mRNA in a subset of thick ascending limb epithelial cells near the macula densa in each developing nephron; after 2 wk the COX-2 gradually waned. These data demonstrate that COX-2 expression is subject to normal developmental regulation and can be sustained over extended periods; they also support the conclusion that metabolites of COX-2 play important roles in the differentiation and early functions of mammalian nephrons.

Aging↗
PubMed1997

Immunohistochemical localization of lipocortin 1 in rat brain is sensitive to pH, freezing, and dehydration.

Lipocortin 1 (LC1, annexin 1) has received considerable attention as a substrate for protein kinases, as a Ca++- and phosphatidylserine-binding protein, and as a mediator of glucocorticoid anti-inflammatory effects. However, there has been confusion over localization of LC1 immunoreactivity (LC1-ir), which reportedly localizes to neurons and/or to astrocytes or microglia in rat brain. To test whether these contradictory data arise from unusual properties of the antigen, we developed a novel brain slice model to determine fixation and staining variables. The specificity of anti-LC1 sera was ensured by pre-absorption and affinity purification with immobilized recombinant LC1. Specific LC1-ir was detected in ramified microglia of brains perfused with acidified aldehydes and embedded in paraffin. However, commonly used immunohistochemical procedures have unexpected profound effects. LC1-ir was eliminated by fixation with neutral/alkaline aldehydes, by freezing before strong acid-aldehyde fixation, or by staining without partial de/rehydration before the primary serum. The sensitivity of LC1 epitopes to proton and water activities may reflect molecular properties important to LC1's roles in vivo. True LC1-ir was not detected in normal neurons or astrocytes.

Animals↗
PubMed1996

An in vitro metronidazole susceptibility test for trichomoniasis using the InPouch TV test.

OBJECTIVE: An efficient anaerobic culture system, the InPouch TV test, was used to determine the susceptibility of Trichomonas vaginalis to metronidazole. Glacial acetic acid was employed as a solvent for metronidazole. METHODS: T vaginalis isolates were cultured from 16 symptomatic female patients. The 11 who responded to oral metronidazole, 250 mg tid for 7 days, were considered as having sensitive trichomonads; the 5 who remained infected after treatment were considered to have resistant organisms. All isolates were cultured for minimum lethal concentrations (MLC). Metronidazole was added to a series of pouches; two-fold dilution of the most concentrated was 50 micrograms/ml and the least was 0.4 micrograms/ml. The inoculum of viable trichomonads was 1 x 105/ml in each pouch. Pouches were incubated at 37 degrees C for 48 h, examined microscopically for motile trichomonads, and then 0.5 ml was subcultured to drug free pouches. After 5 days incubation at 37 degrees C, each subculture and culture were examined microscopically for viable trichomonads. RESULTS: Eleven isolates of T vaginalis from patients responding to metronidazole treatment had MLC between 0.4 to 3.1 micrograms/ml. The MLC from the 5 treatment failure patients were between 12.5 to 50 micrograms/ml. CONCLUSIONS: For the 16 patients in this study, the MLC values determined with the InPouch TV test differentiated between infection caused by metronidazole sensitive and resistant trichomonads. The mean MLC of clinically resistant isolates was approximately eleven fold higher than the mean MLC of clinically sensitive isolates (15 micrograms/ml vs 1.32 micrograms/ml). There was a significant difference between clinically resistant and sensitive isolates (t = 5.47, p < 0.0005). This study suggests that the InPouch TV test could be used for distinguishing between metronidazole resistant and sensitive isolates.

Animals↗
PubMed1996

Laboratory evaluation on the toxic effects of bednets impregnated with permethrin against malaria mosquitos.

In the laboratory, bednets impregnated with 250mg ai/m2 and 500mg ai/m2 permethrin caused respectively the mean mortalities of 86.6% within 13 months and 87.2% within 17 months on laboratory-bred An. sinensis, while they caused average mortalities of 58.3% within 4 months and 73.8% within 10 months on An. dirus respectively. The bioassay results of KT50 and LT50 on the two species showed that KT50 is shorter than LT50 after exposure to the treated bednets. The ratio is 1:2.16 - 1:3.05. It was observed Anopheles had obviously secondary knocked down after exposure to the treated bednets and there is obvious resurgent after Anopheles have been knocked down. When the temperature goes up the resurgence gets shorter, the resurgence rate gets higher and the mortality gets lower. It showed that permethrin has stronger knocking down effect than killing effect.

Animals↗
PubMed1995

A new strategy for enhancing the stability of lyophilized protein: the effect of the reconstitution medium on keratinocyte growth factor.

PURPOSE: Protein stabilization during lyophilization has previously focused on optimization of the formulation as well as the freezing and dehydration process parameters. However, the effect of the reconstitution medium has been largely neglected. We have investigated its effect on aggregate formation using recombinant keratinocyte growth factor (KGF). METHODS: The protein was lyophilized under suboptimal conditions to induce aggregation and precipitation upon reconstitution with water. A series of additives were examined by UV spectrophotometry and size exclusion chromatography (SEC-HPLC) for their effects on decreasing the degree of KGF aggregation and precipitation by the increase in recovery of soluble monomer. RESULTS: Several additives resulted in a significant reduction of aggregation, including sulfated polysaccharides, surfactants, polyphosphates, and amino acids. A similar effect was achieved by adjusting the ionic strength of the reconstitution medium. SEC-HPLC indicated that the amount of soluble monomer was also increased by these additives suggesting that the recovery of the soluble protein correlates with the native, monomeric protein. CONCLUSIONS: These results suggest that optimization of reconstitution conditions will be a useful methodology for increasing the recovery of soluble, active proteins and that for KGF, the recovery of the soluble protein correlates with the native, monomeric form.

Animals↗