Studi Penelusuran (Tracer Study) Alumni Program Studi Pendidikan Non Formal Fakultas Ilmu Pendidikan Universitas Negeri Surabaya Tahun Wisuda 2000 – 2004

Penelitian ini bertujuan untuk mengetahui (1) profil alumni, (2) bidang kerja alumni, (3) kesesuaian bidang kerja dengan program studi, (4) keterampilan sosial alumni, dan (5) saran alumni yang diberikan kepada pengembangan dosen dan lembaga. Penelitian ini menggunakan jenis penelitian deskriptif dengan metode survei. Populasi pada penelitian ini adalah alumni program studi Pendidikan Non Formal Fakultas Ilmu Pendidikan Universitas Negeri Surabaya tahun wisuda 2000-2004 yang berjumlah 56. Penelitian ini menggunakan seluruh populasi sebagai responden penelitian dengan angket hasil penelitian yang didapatkan peneliti berjumlah 48.. Teknik pengumpulan menggunakan metode angket dan teknik analisis data menggunakan analisis deskriptif dengan presentase. Hasil penelitian menunjukkan, (1) Profil alumni dengan presntase tertinggi: IPK (Indeks Prestasi Kumulatif) sebesar 81% dengan predikat sangat memuaskan, sebesar 62% dengan masa studi lebih dari 8 semester, dan lama masa tunggu mendapatkan pekerjaan 35% yaitu  6- 12 bulan.(2) Bidang kerja alumni sebagai tenaga pendidik dan non pendidik. Sebanyak 27% sebagai karyawan Perusahaan dan 25% sebagai guru. (3) Kesesuaian bidang kerja dengan program studi adalah untuk kesesuaian pekerjaan dengan program studi adalah 40% kurang sesuai. (4) keterampilan sosial alumni termasuk dalam kategori sangat baik dengan prosentase 89%. (5) Saran yang diberikan alumni adalah agar ditambahkan praktek – praktek lapangan di berbagai macam tempat dan diberikan keterampilan – keterampilan lain sebagai alternatif untuk alumni ke depannya.   Kata kunci : studi penelusuran, alumni, program studi pendidikan non forma

On the Rate of Convergence for a Characteristic of Multidimensional Birth-Death Process

We consider a multidimensional inhomogeneous birth-death process (BDP) and obtain bounds on the rate of convergence for the corresponding one-dimensional processes

BK channels mediate a novel ionic mechanism that regulates glucose-dependent electrical activity and insulin secretion in mouse pancreatic β-cells

BK channels are large unitary conductance K + channels cooperatively activated by intracellular calcium and membrane depolarisation. We show that BK channels regulate electrical activity in β-cells of mouse pancreatic islets exposed to elevated glucose. In 11.1 m m glucose, the non-peptidyl BK channel blocker paxilline increased the height of β-cell action potentials (APs) by 21 mV without affecting burst- or silent-period durations. In isolated β-cells, paxilline increased AP height by 16 mV without affecting resting membrane potential. In voltage clamp, paxilline blocked a transient component of outward current activated by a short depolarisation, which accounted for at least 90% of the initial outward K + current. This BK current ( I BK ) was blocked by the Ca 2+ channel blockers Cd 2+ (200 μ m ) or nimodipine (1 μ m ), and potentiated by FPL-64176 (1 μ m ). I BK was also 56% blocked by the BK channel blocker iberiotoxin (100 n m ). I BK activated more than 10-fold faster than the delayed rectifier I Kv over the physiological voltage range, and partially inactivated. An AP-like command revealed that I BK activated and deactivated faster than I Kv and accounted for 86% of peak I K , explaining why I BK block increased AP height. A higher amplitude AP-like command, patterned on an AP recorded in 11.1 m m glucose plus paxilline, activated 4-fold more I Kv and significantly increased Ca 2+ entry. Paxilline increased insulin secretion in islets exposed to 11.1 m m glucose by 67%, but did not affect basal secretion in 2.8 m m glucose. These data suggest a modified model of β-cell AP generation where I BK and I Kv coordinate the AP repolarisation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/79246/1/jphysiol.2009.184341.pd

Rad GTPase is essential for the regulation of bone density and bone marrow adipose tissue in mice

The small GTP-binding protein Rad (RRAD, Ras associated with diabetes) is the founding member of the RGK (Rad, Rem, Rem2, and Gem/Kir) family that regulates cardiac voltage-gated Ca2 + channel function. However, its cellular and physiological functions outside of the heart remain to be elucidated. Here we report that Rad GTPase function is required for normal bone homeostasis in mice, as Rad deletion results in significantly lower bone mass and higher bone marrow adipose tissue (BMAT) levels. Dynamic histomorphometry in vivo and primary calvarial osteoblast assays in vitro demonstrate that bone formation and osteoblast mineralization rates are depressed, while in vitro osteoclast differentiation is increased, in the absence of Rad. Microarray analysis revealed that canonical osteogenic gene expression (Runx2, osterix, etc.) is not altered in Rad−/− calvarial osteoblasts; instead robust up-regulation of matrix Gla protein (MGP, + 11-fold), an inhibitor of extracellular matrix mineralization and a protein secreted during adipocyte differentiation, was observed. Strikingly, Rad deficiency also resulted in significantly higher marrow adipose tissue levels in vivo and promoted spontaneous in vitro adipogenesis of primary calvarial osteoblasts. Adipogenic differentiation of wildtype calvarial osteoblasts resulted in the loss of endogenous Rad protein, further supporting a role for Rad in the control of BMAT levels. These findings reveal a novel in vivo function for Rad and establish a role for Rad signaling in the complex physiological control of skeletal homeostasis and bone marrow adiposity

Adult Spiny Mice (\u3ci\u3eAcomys\u3c/i\u3e) Exhibit Endogenous Cardiac Recovery in Response to Myocardial Infarction

Complex tissue regeneration is extremely rare among adult mammals. An exception, however, is the superior tissue healing of multiple organs in spiny mice (Acomys). While Acomys species exhibit the remarkable ability to heal complex tissue with minimal scarring, little is known about their cardiac structure and response to cardiac injury. In this study, we first examined baseline Acomys cardiac anatomy and function in comparison with commonly used inbred and outbred laboratory Mus strains (C57BL6 and CFW). While our results demonstrated comparable cardiac anatomy and function between Acomys and Mus, Acomys exhibited a higher percentage of cardiomyocytes displaying distinct characteristics. In response to myocardial infarction, all animals experienced a comparable level of initial cardiac damage. However, Acomys demonstrated superior ischemic tolerance and cytoprotection in response to injury as evidenced by cardiac functional stabilization, higher survival rate, and smaller scar size 50 days after injury compared to the inbred and outbred mouse strains. This phenomenon correlated with enhanced endothelial cell proliferation, increased angiogenesis, and medium vessel maturation in the peri-infarct and infarct regions. Overall, these findings demonstrate augmented myocardial preservation in spiny mice post-MI and establish Acomys as a new adult mammalian model for cardiac research

Rad GTPase Deletion Atenuates Post-Ischemic Cardiac Dysfunction and Remodeling

The protein Rad interacts with the L-type calcium channel complex to modulate trigger Ca2+ and hence to govern contractility. Reducing Rad levels increases cardiac output. Ablation of Rad also attenuated the inflammatory response following acute myocardial infarction. Future studies to target deletion of Rad in the heart could be conducted to establish a novel treatment paradigm whereby pathologically stressed hearts would be given safe, stable positive inotropic support without arrhythmias and without pathological structural remodeling. Future investigations will also focus on establishing inhibitors of Rad and testing the efficacy of Rad deletion in cardioprotection relative to the time of onset of acute myocardial infarction