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K Fushimi

Publications and source records attributed to K Fushimi.

At least 73 records · Page 4Linked to original sources
PubMed1994

Expression and distribution of aquaporin of collecting duct are regulated by vasopressin V2 receptor in rat kidney.

To examine whether expression and distribution of aquaporin of collecting duct (AQP-CD) are regulated by vasopressin V2 receptor (V2R), we performed immunohistochemical studies with specific antibody against AQP-CD. Normal Wistar rats were divided into four groups and treated for 3 d; control, dehydration, vasopressin V1 receptor (V1R) antagonist (OPC-21268 120 mg/kg), V2R antagonist (OPC-31260 30 mg/kg). At time of death, urine osmolality (Uosm) in the dehydration group (1884 +/- 245 mOsm/kg) was significantly higher than that in the control (938 +/- 91). In the V2R antagonist group, Uosm was significantly decreased to 249 +/- 29, whereas V1R antagonist showed no effect on Uosm. In the control and V1R antagonist groups, immunofluorescence studies showed the AQP-CD staining of both apical membrane and subapical cytoplasm of CD cells of the cortex and the inner medulla. Dehydration increased the immunostaining of both apical membrane and subapical cytoplasm of CD cells of the inner medulla, and the degree of increase was dominant in apical membrane. In the V2R antagonist group, only faint staining of apical membrane and weak labeling of cytoplasm of CD cells of the inner medulla were observed. These changes in the localization and protein amount of AQP-CD by dehydration and V2R antagonist were quantitatively confirmed by immunogold studies and immunoblot analysis of the inner medulla. The present results indicate that the distribution and amount of AQP-CD in the CD cells are regulated by vasopressin V2 receptor.

Animals↗
PubMed1993

Cloning and expression of apical membrane water channel of rat kidney collecting tubule.

Concentrating urine is mandatory for most mammals to prevent water loss from the body. Concentrated urine is produced in response to vasopressin by the transepithelial recovery of water from the lumen of the kidney collecting tubule through highly water-permeable membranes. In this nephron segment, vasopressin regulates water permeability by endo- and exocytosis of water channels from or to the apical membrane. CHIP28 is a water channel in red blood cells and the kidney proximal tubule, but it is not expressed in the collecting tubule. Here we report the cloning of the complementary DNA for WCH-CD, a water channel of the apical membrane of the kidney collecting tubule. WCH-CD is 42% identical in amino-acid sequence to CHIP28. WCH-CD transcripts are detected only in the collecting tubule of the kidney. Immunohistochemically, WCH-CD is localized to the apical region of the kidney collecting tubule cells. Expression of WCH-CD in Xenopus oocytes markedly increases osmotic water permeability. The functional expression and the limited localization of WCH-CD to the apical region of the kidney collecting tubule suggest that WCH-CD is the vasopressin-regulated water channel.

Amino Acid Sequence↗
PubMed1992

Regulation of endothelin-1 production in cultured rat mesangial cells.

We investigated the regulatory mechanisms of endothelin (ET)-1 production in cultured rat mesangial cells (MC), with a special focus on the roles of protein kinase A (PKA)- and protein kinase C (PKC)-mediated signaling systems. Vasoactive agents and growth promoting factors, including platelet-derived growth factor, vasopressin and thrombin, which act through receptors coupled to the phospholipase C-mediated signaling system, as well as phorbol ester and fetal calf serum stimulated ET-1 production. This effect was attenuated in PKC-depleted or H-7 (a PKC inhibitor) treated MC. On the other hand, an increase in intracellular cyclic AMP by forskolin or beta-adrenergic agonist, isoproterenol, which act as anti-mitogenic agents, inhibited serum-stimulated ET-1 production. In addition this effect was mimicked by the addition of 8-bromo-cyclic AMP to the medium. The effect of isoproterenol was abolished by propranolol. H-8, a PKA inhibitor, attenuated the inhibitory effect of forskolin. These findings suggest that ET-1 production in MC is regulated by interaction of both positive and negative signals mediated by PKC- and PKA-dependent mechanisms.

Animals↗
PubMed1992

Organic osmolytes increase cytoplasmic viscosity in kidney cells.

The hypothesis was tested that accumulation of osmolytes by kidney cells grown in hyperosmolar media decreases the rotational and translational mobilities of small polar solutes in the cytosolic compartment. Rotational mobility was measured by the picosecond rotational correlation times (tau c) of 2',7'-bis(2-carboxyethyl)-5(6)carboxylfluorescein (BCECF) by multiharmonic microfluorimetry. In isolated segments of rabbit proximal tubule, thick ascending limb, and cortical collecting duct that were perfused and bathed in 300 mosM media, tau c were in the range 180-250 ps, corresponding to apparent rotational viscosities (eta r) of 1.1-1.5 cP. In cortical collecting tubule, eta r was not influenced by serosal vasopressin. In Madin-Darby canine kidney (MDCK) cells grown in 300-1,200 mosM media, eta r increased progressively by up to a factor of 1.38 +/- 0.03; measurements of tau c and macroscopic viscosity in artificial solutions containing osmolytes supported the hypothesis that the increased eta r was due to accumulation of organic osmolytes. BCECF translational mobility was measured by fluorescence photobleaching recovery using a focused 1.2-microns diameter Ar laser beam at 488 nm. Recovery half-times were 36 +/- 3 (SE) ms (n = 10) in MDCK cells grown in 300 mosM media and 62 +/- 3 ms (n = 10) when grown in 1,200 mosM media. The results suggest that accumulation of osmolytes by renal cells is associated with significantly increased cytosolic viscosity. The increased viscosity would slow enzymatic and transport processes in the cytosolic compartment.

Animals↗
PubMed1991

Construction and evaluation of a frequency-domain epifluorescence microscope for lifetime and anisotropy decay measurements in subcellular domains.

The measurement of time-resolved fluorescence parameters in living cells provides a powerful approach to study cell structure and dynamics. An epifluorescence microscope was constructed to resolve multi-component fluorescence lifetimes and complex anisotropy decay rapidly in labile biological samples. The excitation source consisted of focused, polarized laser light modulated by an impulse-driven Pockels' cell; parallel acquisition of phase angles and modulation amplitudes at more than 40 frequencies (5-250 MHz) was obtained by multi-harmonic cross-correlation detection. Lifetime decay was measured against standard solutions introduced into the light path proximal to the microscope objective. Anisotropy decay was measured by rotation of a Glan-Thompson polarizer in the emission path. Phase reference light was split from the beam proximal to the microscope. Optical components were selected to avoid depolarization and to optimize fluorescence detection efficiency. The dichoric was replaced by a 1 mm square mirror. Fitting routine statistics were optimized for model discrimination in realistic biological samples. Instrument performance was evaluated using fluorescein in H2O/glycerol and H2O/ethylene glycol mixtures and in Swiss 3T3 fibroblasts in monolayer culture. Objective depolarization effects were evaluated by measurement of anisotropy decay using objectives of different numerical aperture. Lifetime and anisotropy decay measured by microscopy (0.5 micron laser spot) agreed with data obtained by cuvette fluorimetry. New biological applications for time-resolved fluorescence microscopy are discussed.

Animals↗
PubMed1991

Heterogeneity in ATP-dependent acidification in endocytic vesicles from kidney proximal tubule. Measurement of pH in individual endocytic vesicles in a cell-free system.

Measurement of membrane transport in suspensions of isolated membrane vesicles provides averaged information over a potentially very heterogeneous vesicle population. To examine the regulatory mechanisms for ATP-dependent acidification, methodology was developed to measure pH in individual endocytic vesicles. Endocytic vesicles from proximal tubule apical membrane of rat kidney were labeled in vivo by intravenous infusion of FITC-dextran (9 kD); a microsomal fraction was obtained from dissected renal cortex by homogenization and differential centrifugation. Vesicles were immobilized on a polylysine coated coverglass and imaged at high magnification by a silicon intensified target camera. ATP-dependent acidification was not influenced by endosome immobilization. Endosome pH was determined from the integrated fluorescence intensity of individual labeled vesicles after background subtraction. Calibration studies with high K and nigericin showed nearly identical fluorescence vs. pH curves for different endosomes with a standard deviation for a single pH measurement in a single endosome of approximately 0.2 pH units. In response to addition of 1 mM MgATP in the presence of K and valinomycin, endosome pH decreased from 7.2 to a mean of 6.4 with a unimodal distribution with width at half-maximum of approximately 1 pH unit. The drop in endosome pH increased and the shape of the distribution changed when the time between FITC-dextran infusion and kidney removal was increased from 5 to 20 min. Differences in ATP-dependent acidification could not be attributed to heterogeneity in passive proton conductance. These results establish a direct method to measure pH in single endocytic vesicles and demonstrate remarkable heterogeneity in ATP-dependent acidification which was interpreted in terms of heterogeneity in the number and/or activity of proton pumps at serial stages of endocytosis.

Adenosine Triphosphate↗
PubMed1991

Low viscosity in the aqueous domain of cell cytoplasm measured by picosecond polarization microfluorimetry.

Information about the rheological characteristics of the aqueous cytoplasm can be provided by analysis of the rotational motion of small polar molecules introduced into the cell. To determine fluid-phase cytoplasmic viscosity in intact cells, a polarization microscope was constructed for measurement of picosecond anisotropy decay of fluorescent probes in the cell cytoplasm. We found that the rotational correlation time (tc) of the probes, 2,7-bis-(2-carboxyethyl)-5-(and-6-)carboxyfluorescein (BCECF), 6-carboxyfluorescein, and 8-hydroxypyrene-1,3,6-trisulfonic acid (HPTS) provided a direct measure of fluid-phase cytoplasmic viscosity that was independent of probe binding. In quiescent Swiss 3T3 fibroblasts, tc values were 20-40% longer than those in water, indicating that the fluid-phase cytoplasm is only 1.2-1.4 times as viscous as water. The activation energy of fluid-phase cytoplasmic viscosity was 4 kcal/mol, which is similar to that of water. Fluid-phase cytoplasmic viscosity was altered by less than 10% upon addition of sucrose to decrease cell volume, cytochalasin B to disrupt cell cytoskeleton, and vasopressin to activate phospholipase C. Nucleoplasmic and peripheral cytoplasmic viscosities were not different. Our results establish a novel method to measure fluid-phase cytoplasmic viscosity, and indicate that fluid-phase cytoplasmic viscosity in fibroblasts is similar to that of free water.

Animals↗
PubMed1991

Solvent drag measurement of transcellular and basolateral membrane NaCl reflection coefficient in kidney proximal tubule.

The NaCl reflection coefficient in proximal tubule has important implications for the mechanisms of near isosmotic volume reabsorption. A new fluorescence method was developed and applied to measure the transepithelial (sigma NaClTE) and basolateral membrane (sigma NaClcl) NaCl reflection coefficients in the isolated proximal straight tubule from rabbit kidney. For sigma NaClTE measurement, tubules were perfused with buffers containing 0 Cl, the Cl-sensitive fluorescent indicator 6-methoxy-N-[3-sulfopropyl] quinolinium and a Cl-insensitive indicator fluorescein sulfonate, and bathed in buffers of differing cryoscopic osmolalities containing NaCl. The transepithelial Cl gradient along the length of the tubule was measured in the steady state by a quantitative ratio imaging technique. A mathematical model based on the Kedem-Katchalsky equations was developed to calculate the axial profile of [Cl] from tubule geometry, lumen flow, water (Pf) and NaCl (PNaCl) permeabilities, and sigma NaClTE. A fit of experimental results to the model gave PNaCl = (2.25 +/- 0.2) x 10(-5) cm/s and sigma NaClTE = 0.98 +/- 0.03 at 23 degrees C. For measurement of sigma NaClbl, tubule cells were loaded with SPQ in the absence of Cl. NaCl solvent drag was measured from the time course of NaCl influx in response to rapid (less than 1 s) Cl addition to the bath solution. With bath-to-cell cryoscopic osmotic gradients of 0, -60, and +30 mosmol, initial Cl influx was 1.23, 1.10, and 1.25 mM/s; a fit to a mathematical model gave sigma NaClbl = 0.97 +/- 0.04. These results indicate absence of NaCl solvent drag in rabbit proximal tubule. The implications of these findings for water and NaCl movement in proximal tubule are evaluated.

Animals↗
PubMed1991

Relationship between vasopressin-sensitive water transport and plasma membrane fluidity in kidney collecting tubule.

The role of plasma membrane fluidity in the regulation of kidney tubule water permeability has been uncertain. We have used new methods to image the fluorescence anisotropy of fluidity-sensitive fluorophores (Fushimi, Dix, and Verkman. Biophys. J. 57: 241-254, 1990) to quantitate membrane fluidity in cells of the vasopressin-sensitive cortical collecting tubule (CCT) and water-impermeable cortical thick ascending limb (CTAL). Isolated tubule segments from rabbit kidney were perfused in vitro, and apical or basolateral plasma membranes were stained with trimethylammonium diphenylhexatriene (TMA-DPH). TMA-DPH anisotropy (r) was imaged quantitatively by an epifluorescence microscope equipped with rotatable polarizers; TMA-DPH nanosecond lifetime (tau) was measured by flash-lamp excitation and gated photomultiplier detection. In CCT, apical membrane r (0.254 +/- 0.003) was similar to basolateral r (0.252 +/- 0.005). Serosal vasopressin at a dose that increased water permeability greater than 10-fold (250 microU/ml) did not affect apical membrane r (delta r = 0.002 +/- 0.003; 7 tubules). A 0.002 change in r was less than that produced by a 2 degrees C temperature variation. In CTAL, apical membrane r was 0.249 +/- 0.002, similar to r from basolateral membrane of proximal tubule (0.24), but much less than that of proximal tubule apical membrane (0.29). These results establish methodology to quantitate fluidity in intact kidney tubule segments and provide the first measurements of plasma membrane fluidity in CTAL and CCT. Our results suggest that regulation of bulk membrane fluidity in CCT apical membrane is not a component of the hydrosmotic action of vasopressin and that low apical membrane fluidity is not responsible for the low water and NH3 permeabilities in CTAL.

Animals↗
PubMed1990

D1-D2 complex of the photosystem II reaction center from spinach. Isolation and partial characterization.

A pigment-protein complex consisting of D1 and D2 proteins, but depleted in the two lower molecular mass components of photosystem II, i.e. cytochrome b-559 and psbI gene product, has been isolated by octyl-beta-D-glucopyranoside treatment of the purified photosystem II reaction center complex from spinach [(1987) Proc. Natl. Acad. Sci. USA 84, 109-112], followed by separation by high performance liquid chromatography using a gel-permeation column (TSK G3000 SW). The isolated complex is photochemically active in the photoreduction of intrinsic pheophytin a under steady-state illumination, in the presence of dithionite and methyl viologen, and exhibits pigment stoichiometries similar to those in the untreated reaction center, indicating that the D1-D2 complex provides the site of primary photochemistry in photosystem II, as well as the principal binding sites of pigments in the reaction center.

Chromatography, Gel↗
PubMed1990

Cell membrane fluidity in the intact kidney proximal tubule measured by orientation-independent fluorescence anisotropy imaging.

Membrane fluidity was measured in the isolated perfused proximal tubule from rabbit kidney. The apical and basolateral plasma membranes of tubule cells were stained separately with the fluidity-sensitive fluorophore trimethylammonium-diphenyl-hexatriene (TMA-DPH) by luminal or bath perfusion. Fluorescence anisotropy (r) of TMA-DPH was mapped with spatial resolution using an epifluorescence microscope (excitation 380 nm, emission greater than 410 nm) equipped with rotatable polarizers and a quantitative imaging system. To measure r without the confounding effects of fluorophore orientation, images were recorded with emission polarizer parallel and perpendicular to a continuum of orientations of the excitation polarizer. The theoretical basis of this approach was developed and its limitations were evaluated by mathematical modeling. The tubule inner surface (brush border) was brightly stained when the lumen was perfused with 1 microM TMA-DPH for 5 min; apical membrane r was 0.281 +/- 0.006 (23 degrees C). Staining of the tubule basolateral membrane by addition of TMA-DPH to the bath gave a significantly lower r of 0.242 +/- 0.010 (P less than 0.005); there was no staining of the brush border membrane. To interpret anisotropy images quantitatively, effects of tubule geometry, TMA-DPH lifetime, fluorescence anisotropy decay, and objective-depolarization were evaluated. Steady-state and time-resolved r and lifetimes in the intact tubule, measured by a nanosecond pulsed microscopy method, were compared with results in isolated apical and basolateral membrane vesicles from rabbit proximal tubule measured by cuvette fluorometry; r was 0.281 (apical membrane) and 0.276 (basolateral membrane) (23 degrees C). These results establish a methodology to quantitate membrane fluidity in the intact proximal tubule, and demonstrate a significantly higher fluidity in the basolateral membrane than in the apical membrane.

Animals↗
PubMed1990

Decreased fractional excretion of urate as an indicator of prerenal azotemia.

Although the fractional excretion of uric acid (FEUA) is known to reflect extracellular fluid volume changes, the diagnostic significance of decreased FEUA in dehydration has not been previously reported. We studied the possible association between low FEUA and acute prerenal azotemia, and its diagnostic value, compared with other traditional indices, in discriminating prerenal azotemia from renal parenchymal causes of acute renal failure. In 65 chronic renal disease patients, 174 FEUA measurements were obtained from 24-hour urine collections. FEUA levels increased as reciprocal serum creatinine levels decreased. All 8 patients with prerenal azotemia showed significantly decreased FEUA values compared with chronic renal disease patients with a comparable degree of serum creatinine elevation, whereas all 7 patients with acute renal failure had FEUA values higher than those of chronic renal disease patients with comparable creatinine levels. FEUA values in prerenal azotemia were distinctly lower than those in acute renal failure (p less than 0.001). Patients with prerenal azotemia showed a lower fractional excretion of sodium, a lower fractional excretion of chloride and renal failure index, and a higher urine-to-plasma creatinine ratio than those with acute renal failure (p less than 0.05). However, these traditional indices were not useful in discriminating between the two conditions. The urine-to-plasma urea nitrogen ratio and the ratio of plasma urea nitrogen to creatinine showed no statistical difference between prerenal azotemia and acute renal failure. We conclude that, in acute azotemia, a decreased FEUA value may represent a reliable indicator of prerenal azotemia in the differential diagnosis of acute renal failure.

Acute Kidney Injury↗
PubMed1987

A comparative study on proteins released from metaphase chromosomes after digestion with restriction endonucleases and deoxyribonuclease I.

Extensive digestion of Chinese hamster metaphase chromosomes with Alu I, Hae III and Hinf I released up to 40 distinct chromosomal proteins. Some of the proteins released by Hae III or Hinf I were enriched in the protein moiety liberated by Alu I but several proteins released by Hae III were not released by Alu I digestion. The amount of chromosomal protein released by deoxyribonuclease I (DNase I) was comparable to that liberated by the three restriction enzymes so far tested, while only four abundant protein species were detectable in the protein moiety released by DNase I. Two of them with molecular weights of 58,000 and 50,000 were also released by the three restriction enzymes and are similar in size to those found previously in the core-like structure of histone-depleted chromosomes.

Animals↗
PubMed1987

[A case of successful surgical treatment of rectal cancer complicated by acute myelomonocytic leukemia].

A 47-year-old man, who had been diagnosed as having acute myelomonocytic leukemia (AMMOL) and had been treated with combination chemotherapy, was admitted to our hospital because he had developed melena. He had been judged to be in complete remission and had shown no signs of recurrence for years, Daunorubicin, vincristine 6-Mercaptopurine and Cyclophosphamide had been administered for maintenance and intensification therapy. He was well until January 1986, when this melena began. A barium enema was given and he was diagnosed as having rectal cancer. Amputation of the rectum and a permanent abdominal colostomy was made safely, mainly because he had been in complete remission, and he recovered normally after the operation. In recent years, the survival of patients with malignancies has improved due to aggressive treatment even in cases of hematological neoplasms. However, the risk of secondary neoplasms in patients treated for cancer has increased. This case suggests that we have to be careful when prescribing treatment for cancer patients, since anti-tumor drugs may have cartinogenic effects.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1982

[A study on anti-T3 and anti-T4 autoantibodies found in two sisters with juvenile hypothyroidism due to Hashimoto's thyroiditis: II. The effect of treatment with L-thyroxine].

We previously reported that two sisters with juvenile hypothyroidism due to Hashimoto's thyroiditis (Case 1: 13 years old, Case 2: 10 years old) had antibodies against thyroid hormones. Treatment was started with 12.5 micrograms of L-T4 per day in Jan. 1980. The doses were gradually increased, and after 1 year of treatment, both patients were clinically euthyroid on 100 micrograms of L-T4 per day, and the heights of Case 1 and of Case 2 had increased by 9 cm and by 10 cm, respectively. Serum TSH levels were decreased from 1088 microU/ml to 1.7 microU/ml in Case 1, and from 1300 microU/ml to 2.1 microU/ml in Case 2. The titers of antithyroglobulin antibodies as measured by solid phase RIA decreased in both patients after the treatment. The bindings of 125I-T3 and of 125I-T4 to sera in the presence of 8-anilino-1-naphthalene sulfonic acid to block binding to TBG (non-treated sera) were markedly higher in the two patients before therapy than those in ten normal controls (11.8% and 52.3% in Case 1, 46.8% and 21.5% in Case 2, and 5.9 +/- 0.6% and 4.1 +/- 0.5% (mean +/- SD) in the controls, respectively). After the 1 year treatment, the bindings of 125I-T3 and 125I-T4 decreased to normal levels in Case 1 (5.8% and 3.8%, respectively). In Case 2, the 125I-T4 binding decreased to the normal level (4.7%), whereas the 125I-T3 binding decreased but still remained above the normal level (10.6%). In order to exclude the interference of endogenous and/or therapeutic thyroid hormones with the binding of labelled hormones to sera, the sera were treated with dextran-coated charcoal at pH3.0 (acid-treated sera). The bindings of 125I-T3 and 125I-T4 to acid-treated sera were clearly higher in both patients before therapy than those in ten normal controls (16.9% and 60.7% in Case 1, 75.0% and 46.4% in Case 2, and 6.9 +/- 0.7% and 6.8 +/- 0.7% (mean +/- SD) in the controls, respectively), and these values were compatible with those from non-treated sera. After the 1 year treatment, however, the results of acid-treated sera were different from those of non-treated sera. That is, the bindings of 125I-T3 and of 125I-T4 to acid-treated sera from both patients decreased but remained above normal levels (9.3% and 26.5% in Case 1, and 29.4% and 22.5% in Case 2, respectively). These results indicate the presence of antibodies against thyroid hormones even in the euthyroid state during L-T4 treatment, and also the data obtained from the non-treated sera were affected by endogenous and/or therapeutic thyroid hormones. The importance of acid-charcoal treatment for the detection of anti-thyroid hormone antibodies during thyroid hormone administration was suggested. In the serum from another sister of the reported patients, we also found unusual T4-binding proteins which were only detected by the acid-charcoal treatment. The implications of decrement of anti-thyroglobulin antibodies and of anti-thyroid hormone antibodies were discussed.

Adolescent↗
PubMed1982

[A study on anti-T3 and anti-T4 autoantibodies found in two sisters with juvenile hypothyroidism due to Hashimoto's thyroiditis (author's transl)].

Anti-thyroid hormone autoantibodies were found in two sisters of short stature (case 1: 13 years old, case 2: 10 years old). Physical examination revealed clinical findings of hypothyroidism with diffuse goiter. A diagnosis of Hashimoto's thyroiditis was made by open biopsy of the thyroid gland in both patients. Serum levels of T3 and T4 were assayed by double antibody radioimmunoassay. In case 1, serum T3 level was 16 ng/dl and serum T4 level was 2.0 microgram/dl. In case 2, serum T3 levels were high (range, 375 approximately 1660 ng/dl), while serum T4 remained at a very low level (0.9 microgram/dl). On the other hand, the level of T3 in case 2 as well as the level of T4 in case 1 was not detectable by a single antibody radioimmunoassay using dextran-coated charcoal or polyethylene glycol separation. In each case, the serum TSH level measured by double antibody radioimmunoassay was extremely high (255 microunits/ml in case 1, 240 microunits/ml in case 2), which was compatible with the clinical features of primary hypothyroidism. Sera from both patients were incubated with 125I-T3 and 125I-T4, followed by precipitation with polyethylene glycol. The binding of 125I-T3 with serum from case 2 and the binding of 125I-T4 with serum from case 1 were markedly high, suggesting the presence of T3- and T4-binding substance(s) in the sera. IgG prepared from the sera of both cases showed marked and specific binding with T3 in case 2 and T4 in case 1. The association constant for T4-antibody in case 1 was 5.2 x 10(8) M-1 and for T3-antibody in case 2 was 5.0 x 10(9) M-1. The binding capacity for T4 was 1.2 ng/ml.IgG and for T3 was 0.3 ng/mg.IgG.

Adolescent↗