Biomedical subjects

S Yamachika

Publications and source records attributed to S Yamachika.

At least 19 recordsLinked to original sources

PubMed2001

Cloning and functional characterization of chicken p160 coactivator family members.

The factors SRC-1, TIF2 and ACTR were identified as interacting with nuclear receptors in a highly ligand-dependent manner. Because the molecular mass of each of these factors is approximately 160 kDa, they are collectively termed p160 coactivators. So far, p160 coactivators have been cloned from human, mouse and Xenopus. We report here the cloning of the chicken homologues of p160 coactivator members. As in human and mouse, chicken has three p160 coactivators. Each gene encodes an approximately 160 kDa protein which exhibits 70-80% amino acid sequence identity to human and mouse p160 coactivators. Chicken p160 coactivators also have the property of interacting with several liganded nuclear receptors. Moreover, we describe an imperfect LXXLL sequence, termed NR box 4, which is located downstream of NR box 3 and conserved between evolutionarily diverse species. The loss of NR box 4 results in a decrease of interaction with the nuclear receptor, which indicates that NR box 4 is required for efficient interaction.

Acetyltransferases↗

PubMed2001

Alteration of antioxidants during the progression of heart disease in streptozotocin-induced diabetic rats.

Involvement of oxidative stress is implicated in the progression of complication of diabetes mellitus. With respect to heart diseases, we have studied role of oxidative stress/antioxidants using rats treated with streptozotocin to induce diabetes (DM). Hemodynamic and echocardiographic measurements showed thickening of the wall and an increase in the internal dimension of the left ventricle (LV) in DM rats at 8th week. Decrease in diastolic posterior wall velocity and rate of LV pressure change, and increase in LV end diastolic pressures also proved cardiac dysfunction. These changes were further developed in DM rats after 12 weeks. Utilizing rat hearts at 8th and 12th weeks, the following estimations were performed. There was a decrease in the activity of Mn-superoxide dismutase (SOD), suggesting abnormal mitochondrial metabolism of reactive oxygen species. The level of glutathione (GSH) decreased concomitant with a decrease in the expression of gamma-glutamylcysteine synthetase (gamma-GCS). The expression of transforming growth factor-beta1 (TGF-beta1), known as a growth factor and a suppressor of GSH synthesis, elevated in DM rat hearts. Immunohistochemical estimation showed an increase in type IV collagen in DM hearts. Collectively, it was suggested a linkage between mitochondrial damage to generate reactive oxygen species and inactivation of Mn-SOD and elevation of the expression of TGF-beta1 to lead suppression of GSH synthesis and induction of fibrous change for the consequent cardiac dysfunction in DM.

Animals↗

PubMed2000

Preserving normal ventricular activation versus atrioventricular delay optimization during pacing: the role of intrinsic atrioventricular conduction and pacing rate.

The purpose of the study was to compare the effects of DDD pacing with optimal AV delay and AAI pacing on the systolic and diastolic performance at rest in patients with prolonged intrinsic AV conduction (first-degree AV block). We studied 17 patients (8 men, aged 69 +/- 9 years) with dual chamber pacemakers implanted for sick sinus syndrome in 15 patients and paroxysmal high degree AV block in 2 patients. Aortic flow and mitral flow were evaluated using Doppler echocardiography. Study protocol included the determination of the optimal AV delay in the DDD mode and comparison between AAI and DDD with optimal AV delay for pacing rate 70/min and 90/min. Stimulus-R interval during AAI (ARI) was 282 +/- 68 ms for rate 70/min and 330 +/- 98 ms for rate 90/min (P < 0.01). The optimal AV delay was 159 +/- 22 ms. AV delay optimization resulted in an increase of an aortic flow time velocity integral (AFTVI) of 16% +/- 9%. At rate 70/min the patients with ARI < or = 270 ms had higher AFTVI in AAI than in DDD (0.214 +/- 0.05 m vs 0.196 +/- 0.05 m, P < 0.01), while the patients with ARI > 270 ms demonstrated greater AFTVI under DDD compared to AAI (0.192 +/- 0.03 m vs 0.166 +/- 0.02 m, P < 0.01). At rate 90/min AFTVI was higher during DDD than AAI (0.183 +/- 0.03 m vs 0.162 +/- 0.03 m, P < 0.01). Mitral flow time velocity integral (MFTVI) at rate 70/min was higher in DDD than in AAI (0.189 +/- 0.05 m vs 0.173 +/- 0.05 m, P < 0.01), while at rate 90/min the difference was not significant in favor of DDD (0.149 +/- 0.05 m vs 0.158 +/- 0.04 m). The results suggest that in patients with first-degree AV block the relative impact of DDD and AAI pacing modes on the systolic performance depends on the intrinsic AV conduction time and on pacing rate.

Aged↗

PubMed2000

Alleles from chromosomes 1 and 3 of NOD mice combine to influence Sjögren's syndrome-like autoimmune exocrinopathy.

OBJECTIVE: NOD mice exhibit at least 2 overlapping autoimmune diseases: autoimmune endocrinopathy (Type I, insulin dependent diabetes) and autoimmune exocrinopathy (Sjogren's syndrome, SS). To date, 18 chromosomal regions have been identified that contribute to development of diabetes in NOD mice; however, genetic mapping of similar susceptibility loci for autoimmune exocrinopathy is just beginning. We investigated if these 2 autoimmune diseases share a genetic predisposition. METHODS: Congenic partner strains of NOD and C57BL/6 mice containing defined genetic intervals influencing susceptibility to diabetes (Idd) were screened for histological and biochemical markers for their effect on the development of SS-like disease. Saliva flow rates, protein concentration, amylase activity, and cysteine protease activity were evaluated. RESULTS: In contrast to the nonsusceptible parental C57BL/6 strain, C57BL/6.NOD Idd5 congenic partner strain, containing a genetic region derived from chromosome 1 of the NOD mouse, exhibited pathophysiological characteristics of autoimmune exocrinopathy. Replacement of individual diabetes susceptibility intervals Idd3, Idd5, Idd13, Idd1, and Idd9, as well as a combination of the Idd3, Idd10, and Idd17 intervals, with resistance alleles had little effect on development of autoimmune exocrinopathy. Conversely, NOD mice, in which the chromosome regions containing both Idd5 and Idd3 have been replaced by intervals derived from C57BL mice, exhibit a reduced pathophysiology associated with SS-like autoimmune exocrinopathy. CONCLUSION: Alleles on chromosomes 1 (Idd5) and 3 (Idd3) in combination appear to greatly influence susceptibility and resistance to development of autoimmune exocrinopathy. The association with certain Idd, but not other Idd loci, indicate that genetic overlap is present but probably not inclusive.

Alleles↗

PubMed1999

An alternative perspective to the immune response in autoimmune exocrinopathy: induction of functional quiescence rather than destructive autoaggression.

Sjögren's syndrome is characterized by dryness of the eyes and the mouth due to mononuclear cell infiltration of the lacrimal and salivary glands. The aetiology is unknown but autoimmunity is considered to play a significant role in the pathogenesis. Recent studies have focused on the fact that tear and salivary flow involves an entire functional system that includes the mucosal surfaces with adnexes (the site of inflammation), efferent nerve signals sent to the midbrain (lacrimal and salivary response region), and afferent neural signals from the brain to the acinar/ductal epithelial structures in the gland. Mononuclear cell infiltration in exocrine glands can lead to glandular destruction, suggested to be mediated through apoptosis. However, the functional impairment of exocrine glands could be regulated by cytokines and/or antibodies against the muscarinic M3 receptor by inhibiting the neural stimulation of the residual glands. This review discusses the possibility that the pathogenesis of Sjögren's syndrome comprises aberrant immune-mediated neuro-hormonal events.

Animals↗

PubMed1999

Chronic Chagas' heart disease in a Japanese-Brazilian traveler. A case report.

A 57-year-old Japanese-Brazilian man, visiting Japan for only 9 days, was admitted to our hospital due to syncope and frequent ventricular premature beats. He grew up in a rural area of Brazil and moved to Sao Paulo in 1959 when he was 20 years old. We suspected chronic Chagas' heart disease, i.e., dilated cardiomyopathy with apical ventricular aneurysm, right bundle branch block with left anterior fascicular block, and various arrhythmias including supraventricular premature beats, ventricular premature beats and non-sustained ventricular tachycardia because he showed typical echo- and electrocardiographic features of the disease. Coronary arteriograms were normal, and left ventriculogram confirmed the existence of apical ventricular aneurysm. A left ventricle biopsy specimen showed hypertrophic cardiac muscle with mild fibrosis. The diagnosis of chronic Chagas' disease was finally confirmed by the demonstration of Trypanosoma cruzi itself in the blood as well as Trypanosoma cruzi antibodies.

Animals↗

PubMed1998

Transfer of human serum IgG to nonobese diabetic Igmu null mice reveals a role for autoantibodies in the loss of secretory function of exocrine tissues in Sjögren's syndrome.

The NOD (nonobese diabetic) mouse has been studied as an animal model for autoimmune insulin-dependent diabetes and Sjögren's syndrome. NOD.Igmu null mice, which lack functional B lymphocytes, develop progressive histopathologic lesions of the submandibular and lachrymal glands similar to NOD mice, but in the absence of autoimmune insulitis and diabetes. Despite the focal appearance of T cells in salivary and lachrymal tissues, NOD.Igmu null mice fail to lose secretory function as determined by stimulation of the muscarinic/cholinergic receptor by the agonist pilocarpine, suggesting a role for B cell autoantibodies in mediating exocrine dryness. Infusion of purified serum IgG or F(ab')2 fragments from parental NOD mice or human primary Sjögren's syndrome patients, but not serum IgG from healthy controls, alters stimulated saliva production, an observation consistent with antibody binding to neural receptors. Furthermore, human patient IgG fractions competitively inhibited the binding of the muscarinic receptor agonist, [3H]quinuclidinyl benzilate, to salivary gland membranes. This autoantibody activity is lost after preadsorption with intact salivary cells. These findings indicate that autoantibodies play an important part in the functional impairment of secretory processes seen in connection with the autoimmune exocrinopathy of Sjögren's syndrome.

Animals↗

PubMed1998

A novel NOD-derived murine model of primary Sjögren's syndrome.

OBJECTIVE: The appearance of autoimmune diabetes prior to autoimmune exocrinopathy in the NOD mouse suggests that it is an excellent model of secondary, but not primary, autoimmune sicca complications. Since the unique major histocompatibility complex (MHC) I-A(g7) expression in NOD mice is essential for the development of insulitis and diabetes in these animals, we investigated exocrine gland function in NOD.B10.H2b mice, which have an MHC congenic to NOD, as a potential model for primary Sjögren's syndrome (SS). METHODS: Histopathologic manifestations of lymphocytic infiltrates into the pancreas and exocrine tissues were examined by light microscopy. Sera were evaluated for the presence of antinuclear antibodies. Saliva, tears, and gland lysates were evaluated for total volume and protein concentration, the aberrant expression and processing of parotid secretory protein, and cysteine protease activity. RESULTS: NOD.B10.H2b mice exhibited the exocrine gland lymphocytic infiltration typical of the SS-like disease and dysfunction observed in NOD mice, but without the insulitis and diabetes. These mice additionally expressed elevated levels of cysteine protease activity (a measure of apoptotic activity) and abnormal expression and cleavage of parotid secretory protein in the submandibular tissues. CONCLUSION: The results of this study suggest that the unique NOD MHC I-A(g7) is not essential for exocrine tissue autoimmunity. Furthermore, the findings indicate that sicca syndrome occurs independently of autoimmune diabetes and that the congenic NOD.B10.H2b mouse represents a novel murine model of primary SS.

Animals↗

PubMed1998

Salivary gland changes in the NOD mouse model for Sjögren's syndrome: is there a non-immune genetic trigger?

Sjögren's syndrome is a systemic autoimmune disease characterized by patient complaints of oral and ocular dryness accompanied by clinical observations of a progressive loss of salivary and lacrimal function, related to the presence of a focal, periductal leukocyte infiltrate. Progress in understanding the mechanisms involved in the development of autoimmune diseases in general, and Sjögren's syndrome specifically, has been generated as a result of renewed interest in animal models, such as the NOD mouse, which mimics autoimmune sialoadenitis. Biochemical analyses have indicated that the salivary glands have reduced beta-adrenergic, muscarinic, and neuropeptide signal transduction responses that correlate to reduced receptor density and the appearance of autoantibodies directed against these and other cell surface proteins. Using the NOD-scid mouse (lacking functional B- and T-lymphocytes) it has been determined that salivary flow rates are normal; however, these animals show abnormal changes in protein biosynthesis with increasing age. Histological evaluation of the submandibular gland from older NOD-scid mice revealed a loss of acinar cells accompanied by a potential increase in the ductal cell component of the tissue. Consistent with this finding, we recently have observed increased levels of cell death-associated cysteine proteases in the submandibular glands of 20 week NOD and NOD-scid mice but not in BALB/c and young NOD controls. Other novel protease activity was detected in the parotid and submandibular glands from NOD mice, which were able to generate the aberrantly processed PSP from purified BALB/c protein. Taken together, these data paint a complex picture of the development of Sjögren's syndrome-like disease in the NOD mouse model. The presence of activated lymphocytes appears to be necessary for the ultimate loss of exocrine gland function, potentially through the loss of tolerance to glandular proteins. However, the findings of high levels of apoptosis and aberrant protein expression in the submandibular gland in the absence of an immune response (NOD-scid) suggests that genetic alterations in glandular homeostasis involving the death program contribute to disease progression or even the initial trigger of autoimmunity.

Animals↗

PubMed1998

Excessive synthesis of matrix metalloproteinases in exocrine tissues of NOD mouse models for Sjögren's syndrome.

OBJECTIVE: Matrix metalloproteinases (MMP) and their substrates, components of the extracellular matrix, regulate environmental signals for cellular differentiation and tissue function. Changes in the levels of these enzymes may influence cell survival as well as pathology involving ectopic apoptosis. Using the non-obese diabetic (NOD) mouse model for Sjögren's syndrome, we evaluated the synthesis and expression of MMP in the exocrine target tissues of autoimmunity. METHODS: NOD, immunodeficient NOD-scid, and nondiabetic NOD.B10.H2b mice were evaluated for MMP activity in their saliva and exocrine gland lysates by gelatin zymography and reverse transcriptase-polymerase chain reaction (RT-PCR). In addition, changes in protein content of saliva and gland lysates were determined by specific Western blot and by enzymatic activity of amylase and cysteine proteases. Mice continuously treated with the MMP inhibitor GM6001 were evaluated from 7 to 20 weeks of age for the contribution of MMP activity to development of these hallmark biochemical markers of Sjogren's syndrome-like disease of NOD mice. RESULTS: Gelatin zymography of whole saliva and gland lysates indicated the presence of increased proteolytic activity, corresponding to proteins with a molecular mass ranging from 50 to 95 kDa, in the saliva of older (> 20 weeks of age) NOD mice as well as NOD.B10.H2b and NOD-scid mice compared to BALB/c controls. Elevated steady state levels of mRNA transcripts for the gelatinases MMP-2 and MMP-9 were detected in total RNA extracted from parotid and submandibular glands by RT-PCR. Despite prophylactic injection of the broad spectrum MMP inhibitor GM6001 into mice beginning at 7 weeks of age and continuing to 20 weeks, development of the autoimmune exocrinopathy was neither stopped nor retarded. CONCLUSION: These observations suggest that excessive MMP activity is associated with autoimmune Sjögren's syndrome-like disease in NOD mice. However, a possible contribution by increased MMP activity in initiation and progression of this autoimmune disease is yet to be elucidated.

Animals↗

PubMed1997

Elevated levels of cysteine protease activity in saliva and salivary glands of the nonobese diabetic (NOD) mouse model for Sjögren syndrome.

Nonobese diabetic (NOD) mice develop an anti-exocrine gland pathology similar to human Sjögren syndrome. Recently, we demonstrated that NOD-scid mice develop severe loss of submandibular acinar cells with concomitant appearance of abnormal isoforms of salivary proteins suggesting de novo enzymatic cleavage. Because these changes may indicate activation of apoptotic proteases, we examined saliva and salivary tissue for cysteine protease activity. Cysteine protease activities were elevated in saliva and gland lysates from 20-week-old NOD and NOD-scid mice as compared with age- and sex-matched BALB/c or 8-week-old NOD mice. This activity appeared in the submandibular glands, but not in the parotid glands. Western blot analyses using antibodies directed against specific apoptotic proteases (interleukin 1beta converting enzyme, Nedd-2, and Apopain/CPP 32) confirmed these findings. Submandibular glands from NOD-scid mice exhibited the greatest increase in proteolytic activity, indicating that infiltrating leukocytes are not responsible for these changes. Western blot analyses also failed to reveal changes in the levels of cystatins (saliva proteins that inhibit protease activity). Thus, increased cysteine protease activity appears to be directly related to submandibular acinar cell loss in NOD-scid mice involving the apoptotic pathway. Additional protease activity in saliva and gland lysates of older NOD and NOD-scid mice, apparently mutually distinct from cysteine proteases, generated an enzymatically cleaved parotid secretory protein. We suggest, therefore, that proteolytic enzyme activity contributes to loss of exocrine gland tolerance by generating abnormally processed protein constituents.

Aging↗

PubMed1997

Usefulness of color Doppler proximal isovelocity surface area method in quantitating valvular regurgitation.

To define the clinical utility of the color Doppler proximal isovelocity surface area (PISA) method for estimating regurgitant stroke volume (SV), 160 regurgitant lesions were evaluated in 104 patients with mitral (MR), aortic (AR), and tricuspid (TR) regurgitation. Regurgitant SV by PISA was calculated as 2 pi R2 x V x (time-velocity integral/peak flow velocity), where R is the radius corresponding to the first blue-red interface velocity of the maximal PISA during the cardiac cycle. The time-velocity integral and peak flow velocity from the continuous-wave Doppler recording of the regurgitant jet were used to correct PISA for phasic variations in regurgitant flow. Fifteen lesions were excluded because of difficulty in tracing the continuous-wave Doppler regurgitant curve. Among 145 remaining regurgitant lesions, PISA was measurable in 50 (78%) of 64 cases of MR and 24 (69%) of 35 cases of TR but in only 12 (26%) of 46 cases of AR (p < 0.001). Regurgitant SV by PISA correlated modestly well with jet area/atrial area in all atrioventricular valve lesions (MR: r = 0.55; TR: r = 0.65; p < 0.001). However, the correlation improved if only central jets were considered (MR: r = 0.70; TR; r = 0.75; p < 0.001). These findings are not unexpected because jet area/atrial area underestimates the true severity of regurgitation in cases of eccentric (wall-impinging) jets. PISA was detected in all severe cases of regurgitation but in only 64% of cases of mild MR, 45% of cases of mild TR, and 6% of cases of mild AR (p < 0.01). The color Doppler PISA method is clinically useful in estimating regurgitant SV in MR and TR, including mild cases, but is less useful in AR.

Adolescent↗

PubMed1997

Calculation of mitral valve area in mitral stenosis using the proximal isovelocity surface area method. Comparison with two-dimensional planimetry and Doppler pressure half time method.

Two-dimensional echocardiographic (2-D) planimetry and the Doppler pressure half-time (PHT) method have been used to estimate mitral valve area (MVA) in patients with mitral stenosis (MS). Recently, the proximal isovelocity surface area (PISA) method has been shown to be accurate for calculating MVA. The purpose of this study was to compare the PISA method with previous methods. Thirty patients with MS were studied; 17 had pure MS, 4 combined mild MR, 6 combined mild AR, and 3 combined MR and AR. Color Doppler flow mapping was performed at an aliasing (blue-red interface) velocity of 14 cm/sec using the zero-baseline shift. MVA was calculated as 2 x 3.14 x R2 x 14 x (theta/180) / PFV, where R is the distance from aliasing to orifice, 14 is the aliasing velocity, theta is the internal angle of the mitral valve, and PFV is the peak flow velocity at the mitral orifice. MVA was also calculated using the 2-D and PHT methods, and compared with the PISA method. MVA calculated using the PISA method correlated well with the 2-D (r=0.90, p < 0.01, SEE = 0.18 cm2) and PHT methods (r=0.82, p < 0.01, SEE = 0.24 cm2). Compared with the 2-D method, the standard error of the estimate of the PISA method was - 0.14+/-0.18 cm2 and the percent error was -10.4+/-18.9%. Compared with the PHT method, the standard error of the estimate of the PISA method was + 0.01+/-0.24 cm2 and the percent error was +3.4+/-34.6%. MVA calculated using the PISA method correlated well with the 2-D and PHT methods in patients with pure MS or with MS combined mild regurgitation. The PISA method may be useful for calculating MVA as an alternative method.

Adult↗

PubMed1993

Angina pectoris caused by dynamic exercise in hypertrophic cardiomyopathy with normal coronary arteries.

To evaluate the relationship between angina pectoris caused by dynamic exercise and the time course of heart rate (HR) and hemodynamics during dynamic exercise in 15 patients with hypertrophic cardiomyopathy (HCM) with normal epicardial coronary arteries, the supine ergometer exercise test was performed during cardiac catheterization. The HCM patients were divided into a chest pain group (n = 6) and a no chest pain group (n = 9) based upon the results of the ergometer exercise test. There was no significant difference in the level of ST-segment depression after exercise in both the chest pain and no chest pain groups (-2.1 +/- 0.6 mm vs -2.6 +/- 1.1 mm, NS). Increase in heart rate (HR) and left ventricular end-diastolic pressure (LVEDP) in the early phase of the exercise test was significantly greater in the chest pain group compared with the no chest pain group. These observations suggest that in HCM patients, the occurrence of exertional chest pain has a close relationship with the rapid increase in HR and LVEDP in the early phase of dynamic exercise, but does not have a relationship with the gradual increase in these parameters.

Angina Pectoris↗

PubMed1992

Loss of nocturnal decline in blood pressure in diabetic patients with autonomic neuropathy.

We investigated loss of the nocturnal decline in blood pressure (BP) and its mechanism in diabetes mellitus with autonomic neuropathy (ANP). BP was measured every 30 min using ambulatory BP recorders in 52 diabetic patients and 11 nondiabetic controls. As an index of autonomic nervous dysfunction, CVRR (the coefficient of variation of the R-R interval on ECGs) and diastolic blood pressure response on standing were measured. Plasma volume (PV) was measured with RISA. The difference between daytime mean BP (09:00 to 13:00) and nighttime mean BP (01:00 to 05:00) was analyzed. The normal control group showed a significant reduction in mean BP during the nighttime (-12.8 +/- 7.5 mmHg) as compared with the DM group (-3.3 +/- 8.6 mmHg, p < 0.001). The diabetic patients with loss of the nocturnal decline in blood pressure showed autonomic nervous dysfunction and increased PV. In conclusion, the nocturnal elevation of blood pressure might result from an imbalance between reduced tone of sympathetic and parasympathetic functions in addition to the postural effect and increased plasma volume present in diabetic patients.

Adult↗

PubMed1990

Beneficial effects of angiotensin-converting enzyme inhibitor on renal function and glucose homeostasis in diabetics with hypertension.

The antihypertensive efficacy of enalapril and its effects on renal function and glucose homeostasis were investigated in 9 hypertensive patients with non-insulin-dependent diabetes mellitus. Enalapril therapy produced a significant fall in blood pressure (BP) (p less than 0.05) and a significant increase in renal blood flow (p less than 0.05) without a change in glomerular filtration rate. Furthermore, fasting plasma glucose was significantly reduced (p less than 0.01). Similarly, M value, as an index of plasma glucose control in diabetes, was significantly reduced from 19.6 to 10.1 (p less than 0.01). These findings suggested that the angiotensin-converting enzyme inhibitor enalapril was effective in reducing BP and improving renal function, and might improve glucose homeostasis in hypertensive diabetics.

Aged↗

PubMed1990

[Paradoxical response of blood pressure to salt loading in renovascular hypertension].

We studied the effect of high salt intake on blood pressure in two cases with renovascular hypertension. They had hypertension with hyperreninemia and marked difference in plasma renin activity between both renal veins. Blood pressure significantly decreased after single oral administration of captopril. Renal arteriogram revealed significant stenosis in the main artery to the left (case 1) and right (case 2) kidney. Blood pressure response was evaluated after seven (case 1) and five (case 2) days of low salt and seven days (both cases) of high salt intake. Mean blood pressure in two patients was significantly decreased (case 1; 118 +/- 5.5 to 108 +/- 6.1 mmHg and case 2; 150 +/- 3.8 to 138 +/- 3.1 mmHg). Plasma renin activity was also decreased (case 1; 6.25 to 0.77 ng/ml/hr and case 2; 22.8 to 6.3 ng/ml/hr). In case 2, blood pressure elevated markedly during low salt intake, compared with blood pressure level during normal salt intake. The results suggest that excessive salt intake in patients with unilateral renovascular hypertension produces blood pressure reduction because of suppression of renin-angiotensin system. We concluded that in patients with unilateral renovascular hypertension dietary sodium depletion may be harmful, whereas salt supplement may have a beneficial effect.

Adult↗

PubMed1989

[Case of sialolithiasis with severe fatty change of the submandibular salivary gland].

We encountered a 57-year-old female with sialolithiasis associated with severe fatty change in the submandibular salivary gland. The submandibular salivary gland was removed under general anesthesia, and the postoperative course was uneventful. Histopathological changes observed in submandibular salivary glands with sialoliths are mainly inflammatory cell infiltration or connective tissue infiltration. On the other hand, increase in fat cells with age has been reported, but these age-related fatty changes are not severe. It was considered that the cause of the fatty change in this case was related to anoxia, which increased with long-term stasis of the duct system that was brought on by the development of the sialolith.

Adipose Tissue↗