PURPOSE: Sleep deprivation induces depressive symptoms. Dexmedetomidine is a α2-adrenoreceptor agonist and this drug possesses sedative, anxiolytic, analgesic, and anesthetic-sparing effect. In this study, the action of dexmedetomidine on sleep deprivation-induced depressive behaviors was investigated using mice. METHODS: For the inducing of sleep deprivation, the mice were placed inside a water cage containing 15 platforms and filled with water up to 1 cm below the platform surface for 7 days. One day after sleep deprivation, dexmedetomidine at the respective dosage (0.5, 1, and 2 μg/kg) was intraperitoneally treated into the mice, one time per a day during 6 days. Then, forced swimming test and tail suspension test were conducted. Immunohistochemistry for tyrosine hydroxylase (TH), 5-hydroxytryptamine (5-HT; serotonin), tryptophan hydroxylase (TPH) and western blot for D1 dopamine receptor were also performed. RESULTS: Sleep deprivation increased the immobility latency in the forced swimming test and tail suspension test. The expressions of TPH, 5-HT, and D1 dopamine receptor were decreased, whereas, TH expression was increased by sleep deprivation. Dexmedetomidine decreased the immobility latency and increased the expressions of TPH, 5-HT, and D1 dopamine receptor, whereas, HT expression was decreased by dexmedetomidine treatment. CONCLUSIONS: In our results, dexmedetomidine alleviated sleep deprivation-induced depressive behaviors by increasing 5-HT synthesis and by decreasing dopamine production with up-regulation of D1 dopamine receptor.
Animals ; Blotting, Western ; Depression ; Dexmedetomidine* ; Dopamine ; Hindlimb Suspension ; Immunohistochemistry ; Mice* ; Physical Exertion ; Receptors, Dopamine ; Serotonin ; Sleep Deprivation ; Tryptophan Hydroxylase ; Tyrosine 3-Monooxygenase ; Up-Regulation ; Water

Nephrogenic diabetes insipidus (NDI) can cause nonobstructive hydronephrosis. Congenital NDI (CNDI) is caused by a genetic mutation. This case report presents a 12-year-old girl who was incidentally diagnosed with nonobstructive hydronephrosis due to NDI caused by AQP2 gene mutation after being evaluated for microscopic hematuria found on routine health examination at school. The patient's medical and family history was unremarkable, and she complained of nocturia only at the time of the clinic visit. Bilateral hydronephrosis on abdominal ultrasonography prompted a water deprivation test, leading to diagnosis of NDI. Genetic study confirmed p.Asn (AAC)123Ser (AGC) in exon 2 of the AQP2 gene. Polyuria and hydronephrosis improved following arginine-vasopressin therapy. CNDI responsive to treatment should be considered as a possible cause of nonobstructive hydroureter.
Ambulatory Care ; Child ; Diabetes Insipidus, Nephrogenic* ; Diagnosis ; Exons ; Female ; Hematuria ; Humans ; Hydronephrosis* ; Nocturia ; Polyuria ; Ultrasonography ; Water Deprivation

Pulmonary Langerhans cell histiocytosis is an uncommon diffuse cystic lung disease in adults. In rare cases, it can involve extrapulmonary organs and lead to endocrine abnormalities such as central diabetes insipidus. A 42-year-old man presented with polyphagia and polydipsia, as well as a dry cough and dyspnea on exertion. Magnetic resonance imaging of the hypothalamic-pituitary system failed to show the posterior pituitary, which is a typical finding in patients with central diabetes insipidus. This condition was confirmed by a water deprivation test, and the patient was also found to have type 2 diabetes mellitus. Computed tomographic scanning of the lungs revealed multiple, irregularly shaped cystic lesions and small nodules bilaterally, with sparing of the costophrenic angles. Lung biopsy through video-assisted thoracoscopic surgery revealed pulmonary Langerhans cell histiocytosis. On a follow-up visit, only 1 year after the patient had quit smoking, clinical and radiological improvement was significant. Here, we report an uncommon case of pulmonary Langerhans cell histiocytosis that simultaneously presented with diabetes insipidus and diabetes mellitus.
Adult* ; Biopsy ; Cough ; Diabetes Insipidus ; Diabetes Insipidus, Neurogenic* ; Diabetes Mellitus* ; Diabetes Mellitus, Type 2 ; Dyspnea ; Follow-Up Studies ; Histiocytosis, Langerhans-Cell* ; Humans ; Lung ; Lung Diseases ; Magnetic Resonance Imaging ; Male* ; Polydipsia ; Smoke ; Smoking ; Smoking Cessation ; Thoracic Surgery, Video-Assisted ; Water Deprivation

A 27-year-old male with nonobstructive hydronephrosis was referred from the urology department for polyuria evaluation and management. The patient was hospitalized for urinary tract infection and cystostomy was performed due to neurogenic bladder of unknown origin. The patient was of short stature and had visual impairment. From the interview, we discovered he had been suffering from polyuria and polydipsia for more than 20 years. Urine output was 13 L/day and urine osmolarity was 85 mOsm/kg. The results of a water deprivation test were consistent with central diabetes insipidus. Septo-optic dysplasia (SOD) was observed on brain magnetic resonance imaging (MRI). SOD is a very rare condition characterized by agenesis of the septum pellucidum or corpus callosum, which may cause optic nerve aplasia or hypoplasia, midbrain abnormalities and/or hypopituitarism. After desmopressin treatment, polyuria and hydronephrosis were improved. We report a case of a 27-year-old male diagnosed with SOD including diabetes insipidus, resulting in nonobstructive hydronephrosis.
Adult ; Brain ; Corpus Callosum ; Cystostomy ; Deamino Arginine Vasopressin ; Diabetes Insipidus ; Diabetes Insipidus, Neurogenic* ; Humans ; Hydronephrosis* ; Hypopituitarism ; Magnetic Resonance Imaging ; Male ; Mesencephalon ; Optic Nerve ; Osmolar Concentration ; Polydipsia ; Polyuria ; Septo-Optic Dysplasia* ; Septum Pellucidum ; Urinary Bladder, Neurogenic ; Urinary Tract Infections ; Urology ; Vision Disorders ; Water Deprivation

We report the rare case of an adult who was diagnosed with recurrent multisystem Langerhans cell histiocytosis (LCH) involving the pituitary stalk and lung who present with central diabetes insipidus and was successfully treated with systemic steroids and chemotherapy. A 49-year-old man visited our hospital due to symptoms of polydipsia and polyuria that started 1 month prior. Two years prior to presentation, he underwent excision of right 6th and 7th rib lesions for the osteolytic lesion and chest pain, which were later confirmed to be LCH on pathology. After admission, the water deprivation test was done and the result indicated that he had central diabetes insipidus. Sella magnetic resonance imaging showed a mass on the pituitary stalk with loss of normal bright spot at the posterior lobe of the pituitary. Multiple patchy infiltrations were detected in both lung fields by computed tomography (CT). He was diagnosed with recurrent LCH and was subsequently treated with inhaled desmopressin, systemic steroids, vinblastine, and mercaptopurine. The pituitary mass disappeared after two months and both lungs were clear on chest CT after 11 months. Although clinical remission in multisystem LCH in adults is reportedly rare, our case of adult-onset multisystem LCH was treated successfully with systemic chemotherapy using prednisolone, vinblastine, and 6-mercaptopurine, which was well tolerated.
6-Mercaptopurine ; Adult* ; Chest Pain ; Deamino Arginine Vasopressin ; Diabetes Insipidus ; Diabetes Insipidus, Neurogenic* ; Drug Therapy* ; Histiocytosis, Langerhans-Cell* ; Humans ; Lung ; Magnetic Resonance Imaging ; Middle Aged ; Pathology ; Pituitary Gland ; Polydipsia ; Polyuria ; Prednisolone ; Ribs ; Steroids ; Tomography, X-Ray Computed ; Vinblastine ; Water Deprivation

PURPOSE: Sleep deprivation may exert many negative effects on hippocampus-dependent cognitive function, such as learning and memory. The present study was conducted in order to investigate the effects of repetitive sleep deprivation on cognition, apoptotic neuronal cell death, and cell proliferation in the hippocampus, using mice. METHODS: To induce sleep deprivation, mice were placed in a water cage containing six platforms (3 cm in diameter), surrounded by water up to 1 cm beneath the surface of the platform for 24 h. Mice were randomly divided into four groups (n=20 in each group): control group, 24 h rest after 24 h sleep deprivation group, 48 h rest after 24 h sleep deprivation group, and 72 h rest after 24 h sleep deprivation group. This cycle was continued for 36 days. Novel objective recognition test and immunohistochemistry for 5-bromo-2'-deoxyuridine (BrdU), western blot for expression of Bax, Bcl-2, brain-derived neurotrophic factor (BDNF), and caspase-3 were performed. RESULTS: Results of the novel objective recognition test showed decreased cognition in the 24 h rest after 24 h sleep deprivation group, while a similar effect was observed in other groups, compared to the control group. Increased cell proliferation and enhanced expression of BDNF and Bax protein were observed in the 24 h rest after 24 h sleep deprivation group and the 48 h rest after 24 h sleep deprivation group, compared to the control group. Expression of Bcl-2 showed a decrease in the 24 h and 48 h rest groups, compared to the control group. Expression of caspase-3 in the dentate gyrus of the hippocampus showed a significant increase in the 24 h rest after 24 h sleep deprivation group and in the 48 h rest after 24 h sleep deprivation group, compared to the control group. CONCLUSION: Results of the present study indicate that insufficient rest after sleep deprivation may induce impairment of cognitive function. After sleep deprivation, at least 72 hr of rest time is needed for recovery.
Animals ; Apoptosis ; bcl-2-Associated X Protein ; Blotting, Western ; Brain-Derived Neurotrophic Factor ; Bromodeoxyuridine ; Caspase 3 ; Cell Death ; Cell Proliferation ; Cognition ; Dentate Gyrus ; Hippocampus ; Immunohistochemistry ; Learning ; Memory ; Memory, Short-Term ; Mice ; Neurons ; Sleep Deprivation ; Water

We report a rare case of the concurrent manifestation of central diabetes insipidus (CDI) and type 2 diabetes mellitus (DM). A 56 year-old man was diagnosed as a type 2 DM on the basis of hyperglycemia with polyuria and polydipsia at a local clinic two months ago and started an oral hypoglycemic medication, but resulted in no symptomatic improvement at all. Upon admission to the university hospital, the patient's initial fasting blood sugar level was 140 mg/dL, and he showed polydipsic and polyuric conditions more than 8 L urine/day. Despite the hyperglycemia controlled with metformin and diet, his symptoms persisted. Further investigations including water deprivation test confirmed the coexisting CDI of unknown origin, and the patient's symptoms including an intense thirst were markedly improved by desmopressin nasal spray (10 microg/day). The possibility of a common origin of CDI and type 2 DM is raised in a review of the few relevant adult cases in the literature.
Adult ; Blood Glucose ; Deamino Arginine Vasopressin ; Diabetes Insipidus, Neurogenic ; Diabetes Mellitus, Type 2 ; Diet ; Fasting ; Humans ; Hyperglycemia ; Metformin ; Polydipsia ; Polyuria ; Sodium ; Thirst ; Valproic Acid ; Water Deprivation

We report a rare case of the concurrent manifestation of central diabetes insipidus (CDI) and type 2 diabetes mellitus (DM). A 56 year-old man was diagnosed as a type 2 DM on the basis of hyperglycemia with polyuria and polydipsia at a local clinic two months ago and started an oral hypoglycemic medication, but resulted in no symptomatic improvement at all. Upon admission to the university hospital, the patient's initial fasting blood sugar level was 140 mg/dL, and he showed polydipsic and polyuric conditions more than 8 L urine/day. Despite the hyperglycemia controlled with metformin and diet, his symptoms persisted. Further investigations including water deprivation test confirmed the coexisting CDI of unknown origin, and the patient's symptoms including an intense thirst were markedly improved by desmopressin nasal spray (10 microg/day). The possibility of a common origin of CDI and type 2 DM is raised in a review of the few relevant adult cases in the literature.
Adult ; Blood Glucose ; Deamino Arginine Vasopressin ; Diabetes Insipidus, Neurogenic ; Diabetes Mellitus, Type 2 ; Diet ; Fasting ; Humans ; Hyperglycemia ; Metformin ; Polydipsia ; Polyuria ; Thirst ; Water Deprivation

INTRODUCTION: This study examined the regulatory mechanism underlying the meal-induced changes in the hypothalamic-pituitary-adrenal gland (HPA) axis activity. MATERIALS AND METHODS: Male Sprague-Dawley rats (250-300 g) were hired for two different experiments as follows; 1) rats received either 8% sucrose or 0.2% saccharin ad libitum after 48 h of food deprivation with the gastric fistula closed (real feeding) or opened (sham feeding). 2). rats received 5 ml of intra-oral infusion with 0.2% saccharin or distilled water after 48 h of food deprivation. One hour after food access, all rats were sacrificed by a transcardiac perfusion with 4% paraformaldehyde. The brains were processed for c-Fos immunohistochemistry and the cardiac blood was collected for the plasma corticosterone assay. RESULTS: Real feedings with sucrose or saccharin and sham feeding saccharin but not sucrose, following food deprivation decreased the plasma corticosterone level. c-Fos expression in the nucleus tractus of solitarius (NTS) of the fasted rats was increased by the consumption of sucrose but not saccharin, regardless of the feeding method. On the other hand, the consumption of sucrose or saccharin with real feeding but not the sham, induced c-Fos expression in the paraventricular nucleus (PVN) of the fasted rats. The intra-oral infusion with saccharin or water decreased the plasma corticosterone level of the fasted rats. Intra-oral water infusion increased c-Fos expression in both the PVN and NTS, but saccharin only in the NTS in the fasted rats. CONCLUSION: Neither restoration of the fasting-induced elevation of plasma corticosterone nor the activation of neurons in the PVN and NTS after refeeding requires the palatability of food or the post-ingestive satiety and caloric load. In addition, neuronal activation in the hypothalamic PVN may not be an implication in the restoration of the fasting-induced elevation of the plasma corticosterone by oropharyngeal stimuli of palatable food.
Animals ; Axis, Cervical Vertebra ; Brain ; Corticosterone ; Feeding Methods ; Food Deprivation ; Formaldehyde ; Gastric Fistula ; Hand ; Humans ; Immunohistochemistry ; Male ; Neurons ; Paraventricular Hypothalamic Nucleus ; Perfusion ; Plasma ; Polymers ; Rats ; Rats, Sprague-Dawley ; Saccharin ; Salicylamides ; Solitary Nucleus ; Sucrose ; Water

We report a case of Turner syndrome associated with idiopathic central diabetes insipidus in a 12-year-old girl, who presented with polyuria and polydipsia after a year. The patient was very short and and centrally obese, and was initially diagnosed with Turner syndrome, hyperlipidema, and diabetes mellitus. A water deprivation test revealed central diabetes insipidus, and sellar magnetic resonance imaging (MRI) showed a thickening of the pituitary stalk, with normal high signal intensity in the posterior pituitary gland. Replacement therapy with desmopressin was initiated, and follow-up sellar MRI findings after two years showed spontaneous regression of the thickened pituitary stalk. There are only few reports of concomitant Turner syndrome with central diabetes insipidus worldwide. Further observation is needed in order to disclose the cause of central diabetes insipidus in patients having Turner syndrome.
Child ; Deamino Arginine Vasopressin ; Diabetes Insipidus, Neurogenic ; Diabetes Mellitus ; Follow-Up Studies ; Humans ; Magnetic Resonance Imaging ; Pituitary Gland ; Pituitary Gland, Posterior ; Polydipsia ; Polyuria ; Turner Syndrome ; Water Deprivation