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"Calcium is crucial in governing contractile activities of myofilaments in cardiomyocytes, any defeats in calcium homeostasis of the cells would adversely affect heart pumping action. The characterization of calcium handling properties in human induced pluripotent stem cell-derived cardiomyocytes (iPS-CMCs) is of significant interest and pertinent to the stem cell and cardiac regenerative field because of their potential patient-specific therapeutic use."

"Latar belakang: Halotan, anestetika inhalasi yang poten semakin banyak ditinggalkan karena efek aritmogeniknya. Penelitian di tingkat selular kebanyakan dilakukan pada penyandang hipertermia maligna (MH), membuktikan bahwa halotan mengaktivasi reseptor ryanodin (RyR) pada otot rangka, menyebabkan penglepasan berlebihan Ca2+ dari retikulum sarkoplasmik (SR) ke sitosol, memicu hiperkontraktur otot rangka. Diasumsikan halotan mempunyai efek serupa pada otot jantung. Belum banyak penelitian mengenai efek pemberian Mg2+ terhadap perubahan konsentrasi Ca2+ akibat halotan, meskipun Mg2+ dikenal sebagai obat antiaritmik. Mg2+ diduga menurunkan konsentrasi Ca2+ sitosol dengan cara meningkatkan ambilan kembali ke dalam SR melalui aktivitas SERCA. Metode penelitian: Penelitian ini adalah penelitian eksperimental in vitro, dengan subjek sel kultur miosit jantung tikus. Miosit yang dimuat dengan indikator Indo1 dibagi menjadi lima kelompok. Sel kontrol tidak dipajankan dengan halotan. Kelompok sel lainnya dipajankan dengan halotan berkonsentrasi 2 mM (setara dengan 1 - 3 MAC) selama 5 menit. Pada kelompok 1, setelah dipajankan dengan halotan, pajanan dihentikan dan diperiksa besar emisinya (penghentian menit ke- 0). Selanjutnya pemeriksaan emisi dilakukan setelah penghentian pajanan diteruskan selama 5, 10, 15 dan 20 menit. Sel kelompok 2 dan 3 diberi MgSO4 11 M dan 22 mM setelah pajanan halotan, kelompok 4 dan 5 diberi MgSO4 11 mM dan 22 mM sebelum pajanan halotan. Perubahan konsentrasi Ca2+ sitosol diketahui dengan pemindaian laser menggunakan mikroskop konfokal, dihitung dari perubahan besar emisi pada sel terpajan dengan analisis pixel. Hasil: Halotan meningkatkan konsentrasi Ca2+ sitosol jantung secara bermakna. Pemberian MgSO4 sebelum pajanan halotan tidak mencegah peningkatan konsentrasi Ca2+ sitosol. Pemberian MgSO4 setelah pajanan halotan tidak bermakna menurunkan konsentrasi Ca2+ sitosol, namun ditemukan kecenderungan turunnya konsentrasi Ca2+ sitosol dengan penambahan dosis MgSO4, setara dengan efek penghentian pajanan halotan selama 10 menit. Lima belas menit setelah penghentian pajanan halotan, konsentrasi Ca2+ turun secara bermakna. Dua puluh menit setelah pajanan halotan dihentikan, konsentrasi Ca2+ sitosol telah kembali ke nilai awal. Simpulan: Halotan meningkatkan konsentrasi Ca2+ sitosol jantung. Mg2+ tidak bermakna menurunkan konsentrasi Ca2+ sitosol jantung dan tidak mencegah peningkatan konsentrasi Ca2+ sitosol jantung akibat pajanan halotan. Setelah penghentian pajanan halotan selama 15 menit, konsentrasi Ca2+ sitosol turun secara bermakna.

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Background: Halothane, a potent inhalational anesthetic, has been recognized to cause arrhythmia, probably due to activation of ryanodine receptor (RyR), triggering Ca2+ release from sarcoplasmic reticulum (SR) to the cytosol. The similar mechanism had been known in skeletal muscle of malignant hyperthermia (MH) patients. Mg2+ hypothetically prevents Ca2+ release by inhibition of RyR and increasing Ca2+ reuptake to SR by SERCA activity. Although Mg2+ had been used as an antiarrhythmic agent, the effect on reducing halothane-induced high intracellular Ca2+ concentration is not well studied.

Method: This experimental in vitro study was done on cultured cell of rat cardiomyocytes. Cells divided into 6 groups. 5 groups were exposed to halothane for 5 minutes (at concentration of 2 mM, equal to 1-3 MAC) and one was not. Of the 5 halothane-exposed groups, group 1 received no additional treatment, but observed immediately after discontinuation of halothane exposure, then 5, 10, 15 and 20 minutes after discontinuation. Group 2 and 3 were given 11 mM and 22 mM MgSO4 after halothane exposure, respectively. Group 4 and 5 had the corresponding MgSO4 treatment prior to exposure. The change in cytosolic Ca2+ was observed by a confocal microscope and measured by pixel analysis for the emission.

Results: Halothane increased cytosolic Ca2+ concentration in rat cardiac myocytes, in which was not substantially altered by MgSO4 given before or after the exposure. There was a trend of decreasing Ca2+ concentration with higher dose of Mg2+. MgSO4 of 22 mM decreased cytosolic Ca2+ concentration to the same extent as discontinuation of halothane for 10 minutes. The cytosolic Ca2+ concentration significantly decreased 15 minutes after discontinuation of halothane exposure and the cytosolic Ca2+ concentration returned to the basal level 20 minutes after discontinuation of halothane exposure.

Conclusion: Halothane increases cytosolic Ca2+ concentration in rat cardiac myocytes. Neither pre- nor post-halothane exposure administration of MgSO4 substantially alters this phenomenon. Cytosolic Ca2+ concentration was significantly reduced 15 minutes after discontinuation of halothane exposure."

"This volume covers topics ranging from fundamental aspects of calcium signaling to its clinical implications, in a thoughtful and comprehensive way. It includes discussion of calcium signaling in different mammalian cells, oocytes, zebrafishes and even in plants."

"During three months ,August 1991 until November 1991, the randomized clinical trial study was conducted to elucidate the effect of calcium supplementation on calcium metabolism to prevent bone loss ip postmenopausal women. Thirty four postmeno- pausal women age 55 to 65 years old from RN. 01, Panjunan village, Astanaanyar subdistrict, Bandung regency West Java who had undergone menopause at least five years since last menses were recruited to the study. The subjects were randomly assigned to the treatment (1000 mg calcium/day) and the control groups in a double blind designs.Thirty one subjects who remained in the study consist of sixteen treatment subjects and fifteen control subjects were included in the final data analysis. Baseline data of the study showed no a significant difference for all variables, therefore baseline data were homogenous. Based on two x 24 hours dietary recall methods all subjects had low dietary calcium intake (291.5l mg/ day and 289.32 mg/day).After treatment, based on the laboratory tests show that the serum calcium concentration was significantly increased in the treatment group (p<0.001) and was not significant difference (p=O.596) in the control group. Serum calcium was a significant difference (p<0.001) between the treatment and the control group. Parathyroid hormone level was significantly decreased in the treatment group (p<0.05) and was significantly increased in the control group (p<0.01). There was significant difference (p<0.00l) between the treatment and the control group. Bone loss of radius and ulna were determined by z-ray standard measurement were significantly reduced (p<0.001 and p<0.01, respectively) after 1000 mg calcium supplementation. Alkaline phosphatase was significantly decreased (p<0.001) in the treatment group and was significantly increased in the control group. There was significant difference (p<0.001) between the treatment and the control group. Urinary ca}cium creatinine ratio was not significantly increased (pI0.764 and p=0.0BB) and was not significant difference (p=0.067) in all subjects after treatment. This study support the hypothesis that calcium supplementation can maintain calcium balance, even improved bone density in postmenopausal women."

"Latar belakang : Overtraining berdampak buruk terhadap kesehatan karena dapat menyebabkan kematian mendadak pada atlet muda. Berdasarkan data epidemiologi ditemukan bahwa kejadian kematian mendadak (suddent cardiac death) pada atlet muda, penyebab paling banyak adalah gangguan kardiovaskular. Tubuh melakukan adaptasi terhadap beban berlebih, berupa remodelling (morfologi dan elektrofisiologi). Remodeling elektrofisiologis yaitu perubahan pada gap junction, berupa perubahan ekspresi Cx43 yang yang mengakibatkan gangguan penghantaran konduksi listrik. Selama latihan fisik dapat terbentuk ROS yang akan menginduksi permeabilitas mitokondria sehingga terjadi kebocoran sitokrom c, selanjutnya akan mengaktifkan kaskade apoptosis.Metode : Penelitian ini dilakukan pada 6 jaringan kardiomiosit tikus Wistar kelompok kontrol dan overtraining. Ekspresi Cx43 dan caspase-3 diamati melalui pulasan imunohistokimia dan diukur dengan image J.Hasil : Hasil penelitian ini menunjukkan peningkatan bermakna pada ekspresi Cx43 total overtraining (43644.57±27711.03) dibandingkan kelompok kontrol (13002.37±3705.41). Tidak ditemukan perbedaan bermakna ekspresi caspase-3 pada kedua kelompok meskipun diperoleh hasil lebih tinggi pada kelompok overtraining (14.15%±10.54%) dibandingkan kelompok kontrol (2,63%±3.56%).Kesimpulan : Overtraining meningkatkan ekspresi Cx43 total tetapi tidak terbukti meningkatkan caspase-3 pada kardiomiosit ventrikel kiri tikus.

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Background: overtraining has bad effect for health, overtraining can cause sudden death in young athlete, reports of sudden death incidences in young athlete claim that cardiovascular disease is the cause. The heart can face the excess load by remodeling as it?s adaptation mechanism. There is 2 type remodeling, morphology and electrophysiology. Remodeling electrophysiology is a change on Cx43 expression which can interfere the heart?s electrical conduction. Free radical which formed from physical exercise can induce mitochondrial permeability that lead leakage of cytochrome c, so that so that activate the apoptosis cascade.

Methods: This study conducted on 12 Wistar rat?s cardiomyocytes tissue that divided into control and overtraining group. Cx43 expression and caspase-3 was observed through immunohistochemical staining and measured by image J.

Results: There was significant increase in the expression of Cx43 total overtraining (43644.57 ± 27711.03) compared to the control group (13002.37 ± 3705.41). Found no significant differences in the expression of caspase-3 in both groups although the result was higher in the group of overtraining (14,15% ± 10,54%) compared to the control group (2,63% ± 3,56%).

Conclusion: Overtraining increase total Cx43 expression but not proven to increase caspase-3 in the rat left ventricular cardiomyocytes."